document_title: List of FA Community Shield matches

question_text: how many times have arsenal won the community shield

text: List of FA Community Shield matches

text: Results[edit]

text:
Key

(R)
Replay

§
Title was shared after match finished in a draw

Match decided by a penalty shootout after full-time[C]

Team was established for this match only

text:
FA Community Shield winners

Year
Winner(s)
Score
Runner-up
Venue
Attendance
Ref(s)

1908
Manchester United
1–1
Queens Park Rangers
Stamford Bridge
6,000
[24]

1908 (R)
Manchester United
4–0
Queens Park Rangers
Stamford Bridge
50,000
[25]

1909
Newcastle United
2–0
Northampton Town
Stamford Bridge
7,000
[26]

1910
Brighton and Hove Albion
1–0
Aston Villa
Stamford Bridge
13,000
[27]

1911
Manchester United
8–4
Swindon Town
Stamford Bridge
10,000
[28]

1912
Blackburn Rovers
2–1
Queens Park Rangers
White Hart Lane
7,100
[29]

1913
English Professionals XI
7–2
English Amateurs XI
The Den (original)
15,000[D]
[8]

1920
West Bromwich Albion
2–0
Tottenham Hotspur
White Hart Lane
38,168
[9]

1921
Tottenham Hotspur
2–0
Burnley
White Hart Lane
18,000
[10]

1922
Huddersfield Town
1–0
Liverpool
Old Trafford
20,000
[30]

1923
English Professionals XI
2–0
English Amateurs XI
Stamford Bridge
11,000
[31]

1924
English Professionals XI
3–1
English Amateurs XI
Highbury Stadium
10,000
[32]

1925
English Amateurs XI
6–1
English Professionals XI
White Hart Lane
5,000[D]
[33]

1926
English Amateurs XI
6–3
English Professionals XI
Maine Road
1,500
[34]

1927
Cardiff City
2–1
Corinthian
Stamford Bridge
16,500
[35]

1928
Everton
2–1
Blackburn Rovers
Old Trafford
4,000
[36][37]

1929
English Professionals XI
3–0
English Amateurs XI
The Den (original)
6,000
[38]

1930
Arsenal
2–1
Sheffield Wednesday
Stamford Bridge
18,000
[39]

1931
Arsenal
1–0
West Bromwich Albion
Villa Park
21,276
[40]

1932
Everton
5–3
Newcastle United
St James' Park
10,000
[41]

1933
Arsenal
3–0
Everton
Goodison Park
20,000
[42]

1934
Arsenal
4–0
Manchester City
Highbury Stadium
10,888
[43]

1935
Sheffield Wednesday
1–0
Arsenal
Highbury Stadium
15,000[D]
[44]

1936
Sunderland
2–1
Arsenal
Roker Park
15,000
[45]

1937
Manchester City
2–0
Sunderland
Maine Road
14,000
[46]

1938
Arsenal
2–1
Preston North End
Highbury Stadium
7,233
[47]

1948
Arsenal
4–3
Manchester United
Highbury Stadium
31,000
[48]

1949
Portsmouth
Wolverhampton Wanderers
1–1§
—
Highbury Stadium
35,140
[49]

1950
England World Cup XI
4–2
FA Canadian Touring Team
Stamford Bridge
38,468
[50]

1951
Tottenham Hotspur
2–1
Newcastle United
White Hart Lane
27,760
[51]

1952
Manchester United
4–2
Newcastle United
Old Trafford
11,381
[52]

1953
Arsenal
3–1
Blackpool
Highbury Stadium
39,853
[53]

1954
West Bromwich Albion
Wolverhampton Wanderers
4–4§
—
Molineux Stadium
45,035
[54]

1955
Chelsea
3–0
Newcastle United
Stamford Bridge
12,802
[55]

1956
Manchester United
1–0
Manchester City
Maine Road
30,495
[56]

1957
Manchester United
4–0
Aston Villa
Old Trafford
27,923
[57]

1958
Bolton Wanderers
4–1
Wolverhampton Wanderers
Burnden Park
36,029
[58]

1959
Wolverhampton Wanderers
3–1
Nottingham Forest
Molineux Stadium
32,329
[59]

1960
Burnley
Wolverhampton Wanderers
2–2§
—
Turf Moor
19,873
[60]

1961
Tottenham Hotspur
3–2
FA Select XI
White Hart Lane
36,593
[13]

1962
Tottenham Hotspur
5–1
Ipswich Town
Portman Road
20,067
[61]

1963
Everton
4–0
Manchester United
Goodison Park
54,844
[62]

1964
Liverpool
West Ham United
2–2§
—
Anfield
38,858
[63]

1965
Liverpool
Manchester United
2–2§
—
Old Trafford
48,502
[64]

1966
Liverpool
1–0
Everton
Goodison Park
63,329
[65]

1967
Manchester United
Tottenham Hotspur
3–3§
—
Old Trafford
54,106
[66]

1968
Manchester City
6–1
West Bromwich Albion
Maine Road
35,510
[67]

1969
Leeds United
2–1
Manchester City
Elland Road
39,835
[68]

1970
Everton
2–1
Chelsea
Stamford Bridge
43,547
[69]

1971
Leicester City
1–0
Liverpool
Filbert Street
25,104
[70]

1972
Manchester City
1–0
Aston Villa
Villa Park
34,859
[71]

1973
Burnley
1–0
Manchester City
Maine Road
23,988
[72]

1974
Liverpool
1–1[E]
Leeds United
Wembley Stadium (original)
67,000
[73]

1975
Derby County
2–0
West Ham United
Wembley Stadium (original)
59,000
[74]

1976
Liverpool
1–0
Southampton
Wembley Stadium (original)
76,500
[75]

1977
Liverpool
Manchester United
0–0§
—
Wembley Stadium (original)
82,000
[76]

1978
Nottingham Forest
5–0
Ipswich Town
Wembley Stadium (original)
68,000
[77]

1979
Liverpool
3–1
Arsenal
Wembley Stadium (original)
92,800
[78]

1980
Liverpool
1–0
West Ham United
Wembley Stadium (original)
90,000
[79]

1981
Aston Villa
Tottenham Hotspur
2–2§
—
Wembley Stadium (original)
92,500
[80]

1982
Liverpool
1–0
Tottenham Hotspur
Wembley Stadium (original)
82,500
[81]

1983
Manchester United
2–0
Liverpool
Wembley Stadium (original)
92,000
[82]

1984
Everton
1–0
Liverpool
Wembley Stadium (original)
100,000
[83]

1985
Everton
2–0
Manchester United
Wembley Stadium (original)
82,000
[84]

1986
Everton
Liverpool
1–1§
—
Wembley Stadium (original)
88,231
[85]

1987
Everton
1–0
Coventry City
Wembley Stadium (original)
88,000
[86]

1988
Liverpool
2–1
Wimbledon
Wembley Stadium (original)
54,887
[87]

1989
Liverpool
1–0
Arsenal
Wembley Stadium (original)
63,149
[88]

1990
Liverpool
Manchester United
1–1§
—
Wembley Stadium (original)
66,558
[89]

1991
Arsenal
Tottenham Hotspur
0–0§
—
Wembley Stadium (original)
65,483
[90]

1992
Leeds United
4–3
Liverpool
Wembley Stadium (original)
61,291
[91]

1993
Manchester United
1–1[F]
Arsenal
Wembley Stadium (original)
66,519
[92]

1994
Manchester United
2–0
Blackburn Rovers
Wembley Stadium (original)
60,402
[93]

1995
Everton
1–0
Blackburn Rovers
Wembley Stadium (original)
40,149
[94]

1996
Manchester United
4–0
Newcastle United
Wembley Stadium (original)
73,214
[95]

1997
Manchester United
1–1[G]
Chelsea
Wembley Stadium (original)
73,636
[96]

1998
Arsenal
3–0
Manchester United
Wembley Stadium (original)
67,342
[97]

1999
Arsenal
2–1
Manchester United
Wembley Stadium (original)
70,185
[98][99]

2000
Chelsea
2–0
Manchester United
Wembley Stadium (original)
65,148
[100][101]

2001
Liverpool
2–1
Manchester United
Millennium Stadium
70,227
[102][103]

2002
Arsenal
1–0
Liverpool
Millennium Stadium
67,337
[104]

2003
Manchester United
1–1[H]
Arsenal
Millennium Stadium
59,923
[105][106]

2004
Arsenal
3–1
Manchester United
Millennium Stadium
63,317
[107]

2005
Chelsea
2–1
Arsenal
Millennium Stadium
58,014
[108]

2006
Liverpool
2–1
Chelsea
Millennium Stadium
56,275
[109]

2007
Manchester United
1–1[I]
Chelsea
Wembley Stadium (new)
80,731
[110]

2008
Manchester United
0–0[J]
Portsmouth
Wembley Stadium (new)
84,808
[111]

2009
Chelsea
2–2[K]
Manchester United
Wembley Stadium (new)
85,896
[112]

2010
Manchester United
3–1
Chelsea
Wembley Stadium (new)
84,623
[113]

2011
Manchester United
3–2
Manchester City
Wembley Stadium (new)
77,169
[114]

2012
Manchester City
3–2
Chelsea
Villa Park[L]
36,394
[115]

2013
Manchester United
2–0
Wigan Athletic
Wembley Stadium (new)
80,235
[116]

2014
Arsenal
3–0
Manchester City
Wembley Stadium (new)
71,523
[117]

2015
Arsenal
1–0
Chelsea
Wembley Stadium (new)
85,437
[118]

2016
Manchester United
2–1
Leicester City
Wembley Stadium (new)
85,437
[15]

2017
Arsenal
1–1[M]
Chelsea
Wembley Stadium (new)
83,325
[21]

text: Results by club[edit]

text: Teams shown in italics are no longer in existence, or were established only for the purpose of playing in these matches.

text:
FA Community Shield winners by club

Club
Wins
Last final won
Runners-up
Last final lost
Total appearances

Manchester United
21
2016
9
2009
30

Arsenal
15
2017
7
2005
22

Liverpool
15
2006
6
2002
21

Everton
9
1995
2
1966
11

Tottenham Hotspur
7
1991
2
1982
9

Chelsea
4
2009
8
2017
12

Manchester City
4
2012
6
2014
10

English Professionals XI
4
1929
2
1926
6

Wolverhampton Wanderers
4
1960
1
1958
5

English Amateurs XI
2
1926
4
1929
6

West Bromwich Albion
2
1954
2
1968
4

Burnley
2
1973
1
1921
3

Leeds United
2
1992
1
1974
3

Newcastle United
1
1909
5
1996
6

Aston Villa
1
1981
3
1972
4

Blackburn Rovers
1
1912
3
1995
4

West Ham United
1
1964
2
1980
3

Leicester City
1
1971
1
2016
2

Nottingham Forest
1
1978
1
1959
2

Portsmouth
1
1949
1
2008
2

Sheffield Wednesday
1
1935
1
1930
2

Sunderland
1
1936
1
1937
2

Bolton Wanderers
1
1958
0
&
—

1

Brighton and Hove Albion
1
1910
0
&
—

1

Cardiff City
1
1927
0
&
—

1

Derby County
1
1975
0
&
—

1

English World Cup XI
1
1950
0
&
—

1

Huddersfield Town
1
1922
0
&
—

1

Ipswich Town
0
&
—

2
1978
2

Queens Park Rangers
0
&
—

2
1912
2

Blackpool
0
&
—

1
1953
1

Corinthian
0
&
—

1
1927
1

Coventry City
0
&
—

1
1987
1

English FA Canadian Touring XI
0
&
—

1
1950
1

FA Select XI
0
&
—

1
1961
1

Northampton Town
0
&
—

1
1909
1

Preston North End
0
&
—

1
1938
1

Southampton
0
&
—

1
1976
1

Swindon Town
0
&
—

1
1911
1

Wigan Athletic
0
&
—

1
2013
1

Wimbledon
0
&
—

1
1988
1

text: Notes[edit]

text:
Jump up ^ From 2001–2006, the Millennium Stadium was the venue for Shield matches while the new Wembley Stadium was being constructed.[4] In 2012, the match was held at Villa Park because Wembley was hosting the Olympic football tournament.[5]
Jump up ^ Manchester United won 17 titles outright and shared 4 titles.[15]
Jump up ^ If the match finishes in a draw after 90 minutes, no extra time is played and the teams proceed directly to a penalty shootout.[22][23]
^ Jump up to: a b c This attendance figure is not exact and is only an approximation.
Jump up ^ Liverpool won the 1974 match 6–5 in a penalty shootout.
Jump up ^ Manchester United won the 1993 match 5–4 in a penalty shootout.
Jump up ^ Manchester United won the 1997 match 4–2 in a penalty shootout.
Jump up ^ Manchester United won the 2003 match 4–3 in a penalty shootout.
Jump up ^ Manchester United won the 2007 match 3–0 in a penalty shootout.
Jump up ^ Manchester United won the 2008 match 3–1 in a penalty shootout.
Jump up ^ Chelsea won the 2009 match 4–1 in a penalty shootout.
Jump up ^ Villa Park replaced Wembley Stadium as the venue for the 2012 Community Shield match due to the latter's hosting of the Olympic football tournament at the time.[5]
Jump up ^ Arsenal won the 2017 match 4–1 in a penalty shootout.

tag: ol


document_title: DNA

question_text: who proposed the double helical model of dna

question_tokens: who proposed the double helical model of dna

root

text: DNA

text: Properties

text: DNA is a long polymer made from repeating units called nucleotides.[6][7] The structure of DNA is dynamic along its length, being capable of coiling into tight loops, and other shapes.[8] In all species it is composed of two helical chains, bound to each other by hydrogen bonds. Both chains are coiled round the same axis, and have the same pitch of 34 ångströms (3.4 nanometres). The pair of chains has a radius of 10 ångströms (1.0 nanometre).[9] According to another study, when measured in a different solution, the DNA chain measured 22 to 26 ångströms wide (2.2 to 2.6 nanometres), and one nucleotide unit measured 3.3 Å (0.33 nm) long.[10] Although each individual nucleotide repeating unit is very small, DNA polymers can be very large molecules containing millions to hundreds of millions of nucleotides. For instance, the DNA in the largest human chromosome, chromosome number 1, consists of approximately 220 million base pairs[11] and would be 85 mm long if straightened.

tag: p

text: In living organisms, DNA does not usually exist as a single molecule, but instead as a pair of molecules that are held tightly together.[12][13] These two long strands entwine like vines, in the shape of a double helix. The nucleotide contains both a segment of the backbone of the molecule (which holds the chain together) and a nucleobase (which interacts with the other DNA strand in the helix). A nucleobase linked to a sugar is called a nucleoside and a base linked to a sugar and one or more phosphate groups is called a nucleotide. A polymer comprising multiple linked nucleotides (as in DNA) is called a polynucleotide.[14]

text: The backbone of the DNA strand is made from alternating phosphate and sugar residues.[15] The sugar in DNA is 2-deoxyribose, which is a pentose (five-carbon) sugar. The sugars are joined together by phosphate groups that form phosphodiester bonds between the third and fifth carbon atoms of adjacent sugar rings. These asymmetric bonds mean a strand of DNA has a direction. In a double helix, the direction of the nucleotides in one strand is opposite to their direction in the other strand: the strands are antiparallel. The asymmetric ends of DNA strands are said to have a directionality of five prime (5′) and three prime (3′), with the 5′ end having a terminal phosphate group and the 3′ end a terminal hydroxyl group. One major difference between DNA and RNA is the sugar, with the 2-deoxyribose in DNA being replaced by the alternative pentose sugar ribose in RNA.[13]

text: The DNA double helix is stabilized primarily by two forces: hydrogen bonds between nucleotides and base-stacking interactions among aromatic nucleobases.[17] In the aqueous environment of the cell, the conjugated π bonds of nucleotide bases align perpendicular to the axis of the DNA molecule, minimizing their interaction with the solvation shell. The four bases found in DNA are adenine (A), cytosine (C), guanine (G) and thymine (T). These four bases are attached to the sugar-phosphate to form the complete nucleotide, as shown for adenosine monophosphate. Adenine pairs with thymine and guanine pairs with cytosine. It was represented by A-T base pairs and G-C base pairs.[18][19]

text: Nucleobase classification

text: The nucleobases are classified into two types: the purines, A and G, being fused five- and six-membered heterocyclic compounds, and the pyrimidines, the six-membered rings C and T.[13] A fifth pyrimidine nucleobase, uracil (U), usually takes the place of thymine in RNA and differs from thymine by lacking a methyl group on its ring. In addition to RNA and DNA, many artificial nucleic acid analogues have been created to study the properties of nucleic acids, or for use in biotechnology.[20]

text: Non canonical bases

text: Uracil is not usually found in DNA, occurring only as a breakdown product of cytosine. However, in several bacteriophages, Bacillus subtilis bacteriophages PBS1 and PBS2 and Yersinia bacteriophage piR1-37, thymine has been replaced by uracil.[21] Another phage - Staphylococcal phage S6 - has been identified with a genome where thymine has been replaced by uracil.[22]

text: 5-hydroxymethyldeoxyuridine,(hm5dU) is also known to replace thymidine in several genomes including the Bacillus phages SPO1, ϕe, SP8, H1, 2C and SP82. Another modified uracil - 5-dihydroxypentauracil – has also been described.[23]

text: Base J (beta-d-glucopyranosyloxymethyluracil), a modified form of uracil, is also found in several organisms: the flagellates Diplonema and Euglena, and all the kinetoplastid genera.[24] Biosynthesis of J occurs in two steps: in the first step, a specific thymidine in DNA is converted into hydroxymethyldeoxyuridine; in the second, HOMedU is glycosylated to form J.[25] Proteins that bind specifically to this base have been identified.[26][27][28] These proteins appear to be distant relatives of the Tet1 oncogene that is involved in the pathogenesis of acute myeloid leukemia.[29] J appears to act as a termination signal for RNA polymerase II.[30][31]

text: In 1976 a bacteriophage - S-2L - which infects species of the genus Synechocystis was found to have all the adenosine bases within its genome replaced by 2,6-diaminopurine.[32] In 2016 deoxyarchaeosine was found to be present in the genomes of several bacteria and the Escherichia phage 9g.[33]

text: Modified bases also occur in DNA. The first of these recognised was 5-methylcytosine which was found in the genome of Mycobacterium tuberculosis in 1925.[34] The complete replacement of cytosine by 5-glycosylhydroxymethylcytosine in T even phages (T2, T4 and T6) was observed in 1953[35] In the genomes of Xanthomonas oryzae bacteriophage Xp12 and halovirus FH the full complement of cystosine has been replaced by 5-methylcytosine.[36][37] 6N-methyadenine was discovered to be present in DNA in 1955.[38] N6-carbamoyl-methyladenine was described in 1975.[39] 7-methylguanine was described in 1976.[40] N4-methylcytosine in DNA was described in 1983.[41] In 1985 5-hydroxycytosine was found in the genomes of the Rhizobium phages RL38JI and N17.[42] α-putrescinylthymine occurs in both the genomes of the Delftia phage ΦW-14 and the Bacillus phage SP10.[43] α-glutamylthymidine is found in the Bacillus phage SP01 and 5-dihydroxypentyluracil is found in the Bacillus phage SP15.

text: The reason for the presence of these non canonical bases in DNA is not known. It seems likely that at least part of the reason for their presence in bacterial viruses (phages) is to avoid the restriction enzymes present in bacteria. This enzyme system acts at least in part as a molecular immune system protecting bacteria from infection by viruses.

text: This does not appear to be the entire story. Four modifications to the cytosine residues in human DNA have been reported.[44] These modifications are the addition of methyl (CH3)-, hydroxymethyl (CH2OH)-, formyl (CHO)- and carboxyl (COOH)- groups. These modifications are thought to have regulatory functions.

text: Listing of non canonical bases found in DNA

text: Seventeen non canonical bases are known to occur in DNA. Most of these are modifications of the canonical bases plus uracil.

text:
Modified Adenosine

N6-carbamoyl-methyladenine
N6-methyadenine

Modified Guanine

7-Methylguanine

Modified Cytosine

N4-Methylcytosine
5-Carboxylcytosine
5-Formylcytosine
5-Glycosylhydroxymethylcytosine
5-Hydroxycytosine
5-Methylcytosine

Modified Thymidine

α-Glutamythymidine
α-Putrescinylthymine

Uracil and modifications

Base J
Uracil
5-Dihydroxypentauracil
5-Hydroxymethyldeoxyuracil

Others

Deoxyarchaeosine
2,6-Diaminopurine

tag: ul

text: Grooves

text: Twin helical strands form the DNA backbone. Another double helix may be found tracing the spaces, or grooves, between the strands. These voids are adjacent to the base pairs and may provide a binding site. As the strands are not symmetrically located with respect to each other, the grooves are unequally sized. One groove, the major groove, is 22 Å wide and the other, the minor groove, is 12 Å wide.[45] The width of the major groove means that the edges of the bases are more accessible in the major groove than in the minor groove. As a result, proteins such as transcription factors that can bind to specific sequences in double-stranded DNA usually make contact with the sides of the bases exposed in the major groove.[46] This situation varies in unusual conformations of DNA within the cell (see below), but the major and minor grooves are always named to reflect the differences in size that would be seen if the DNA is twisted back into the ordinary B form.

text: Base pairing

text: In a DNA double helix, each type of nucleobase on one strand bonds with just one type of nucleobase on the other strand. This is called complementary base pairing. Here, purines form hydrogen bonds to pyrimidines, with adenine bonding only to thymine in two hydrogen bonds, and cytosine bonding only to guanine in three hydrogen bonds. This arrangement of two nucleotides binding together across the double helix is called a Watson-Crick base pair. Another type of base pairing is Hoogsteen base pairing where two hydrogen bonds form between guanine and cytosine.[47] As hydrogen bonds are not covalent, they can be broken and rejoined relatively easily. The two strands of DNA in a double helix can thus be pulled apart like a zipper, either by a mechanical force or high temperature.[48] As a result of this base pair complementarity, all the information in the double-stranded sequence of a DNA helix is duplicated on each strand, which is vital in DNA replication. This reversible and specific interaction between complementary base pairs is critical for all the functions of DNA in living organisms.[7]

tag: table

text: The two types of base pairs form different numbers of hydrogen bonds, AT forming two hydrogen bonds, and GC forming three hydrogen bonds (see figures, right). DNA with high GC-content is more stable than DNA with low GC-content.

text: As noted above, most DNA molecules are actually two polymer strands, bound together in a helical fashion by noncovalent bonds; this double-stranded (dsDNA) structure is maintained largely by the intrastrand base stacking interactions, which are strongest for G,C stacks. The two strands can come apart – a process known as melting – to form two single-stranded DNA (ssDNA) molecules. Melting occurs at high temperature, low salt and high pH (low pH also melts DNA, but since DNA is unstable due to acid depurination, low pH is rarely used).

text: The stability of the dsDNA form depends not only on the GC-content (% G,C basepairs) but also on sequence (since stacking is sequence specific) and also length (longer molecules are more stable). The stability can be measured in various ways; a common way is the "melting temperature", which is the temperature at which 50% of the ds molecules are converted to ss molecules; melting temperature is dependent on ionic strength and the concentration of DNA. As a result, it is both the percentage of GC base pairs and the overall length of a DNA double helix that determines the strength of the association between the two strands of DNA. Long DNA helices with a high GC-content have stronger-interacting strands, while short helices with high AT content have weaker-interacting strands.[49] In biology, parts of the DNA double helix that need to separate easily, such as the TATAAT Pribnow box in some promoters, tend to have a high AT content, making the strands easier to pull apart.[50]

text: In the laboratory, the strength of this interaction can be measured by finding the temperature necessary to break the hydrogen bonds, their melting temperature (also called Tm value). When all the base pairs in a DNA double helix melt, the strands separate and exist in solution as two entirely independent molecules. These single-stranded DNA molecules have no single common shape, but some conformations are more stable than others.[51]

text: Sense and antisense

text: A DNA sequence is called "sense" if its sequence is the same as that of a messenger RNA copy that is translated into protein.[52] The sequence on the opposite strand is called the "antisense" sequence. Both sense and antisense sequences can exist on different parts of the same strand of DNA (i.e. both strands can contain both sense and antisense sequences). In both prokaryotes and eukaryotes, antisense RNA sequences are produced, but the functions of these RNAs are not entirely clear.[53] One proposal is that antisense RNAs are involved in regulating gene expression through RNA-RNA base pairing.[54]

text: A few DNA sequences in prokaryotes and eukaryotes, and more in plasmids and viruses, blur the distinction between sense and antisense strands by having overlapping genes.[55] In these cases, some DNA sequences do double duty, encoding one protein when read along one strand, and a second protein when read in the opposite direction along the other strand. In bacteria, this overlap may be involved in the regulation of gene transcription,[56] while in viruses, overlapping genes increase the amount of information that can be encoded within the small viral genome.[57]

text: Supercoiling

text: DNA can be twisted like a rope in a process called DNA supercoiling. With DNA in its "relaxed" state, a strand usually circles the axis of the double helix once every 10.4 base pairs, but if the DNA is twisted the strands become more tightly or more loosely wound.[58] If the DNA is twisted in the direction of the helix, this is positive supercoiling, and the bases are held more tightly together. If they are twisted in the opposite direction, this is negative supercoiling, and the bases come apart more easily. In nature, most DNA has slight negative supercoiling that is introduced by enzymes called topoisomerases.[59] These enzymes are also needed to relieve the twisting stresses introduced into DNA strands during processes such as transcription and DNA replication.[60]

text: Alternative DNA structures

text: DNA exists in many possible conformations that include A-DNA, B-DNA, and Z-DNA forms, although, only B-DNA and Z-DNA have been directly observed in functional organisms.[15] The conformation that DNA adopts depends on the hydration level, DNA sequence, the amount and direction of supercoiling, chemical modifications of the bases, the type and concentration of metal ions, and the presence of polyamines in solution.[61]

text: The first published reports of A-DNA X-ray diffraction patterns—and also B-DNA—used analyses based on Patterson transforms that provided only a limited amount of structural information for oriented fibers of DNA.[62][63] An alternative analysis was then proposed by Wilkins et al., in 1953, for the in vivo B-DNA X-ray diffraction-scattering patterns of highly hydrated DNA fibers in terms of squares of Bessel functions.[64] In the same journal, James Watson and Francis Crick presented their molecular modeling analysis of the DNA X-ray diffraction patterns to suggest that the structure was a double-helix.[9]

text: Although the B-DNA form is most common under the conditions found in cells,[65] it is not a well-defined conformation but a family of related DNA conformations[66] that occur at the high hydration levels present in living cells. Their corresponding X-ray diffraction and scattering patterns are characteristic of molecular paracrystals with a significant degree of disorder.[67][68]

text: Compared to B-DNA, the A-DNA form is a wider right-handed spiral, with a shallow, wide minor groove and a narrower, deeper major groove. The A form occurs under non-physiological conditions in partly dehydrated samples of DNA, while in the cell it may be produced in hybrid pairings of DNA and RNA strands, and in enzyme-DNA complexes.[69][70] Segments of DNA where the bases have been chemically modified by methylation may undergo a larger change in conformation and adopt the Z form. Here, the strands turn about the helical axis in a left-handed spiral, the opposite of the more common B form.[71] These unusual structures can be recognized by specific Z-DNA binding proteins and may be involved in the regulation of transcription.[72]

text: Alternative DNA chemistry

text: For many years exobiologists have proposed the existence of a shadow biosphere, a postulated microbial biosphere of Earth that uses radically different biochemical and molecular processes than currently known life. One of the proposals was the existence of lifeforms that use arsenic instead of phosphorus in DNA. A report in 2010 of the possibility in the bacterium GFAJ-1, was announced,[73][73][74] though the research was disputed,[74][75] and evidence suggests the bacterium actively prevents the incorporation of arsenic into the DNA backbone and other biomolecules.[76]

text: Quadruplex structures

text: At the ends of the linear chromosomes are specialized regions of DNA called telomeres. The main function of these regions is to allow the cell to replicate chromosome ends using the enzyme telomerase, as the enzymes that normally replicate DNA cannot copy the extreme 3′ ends of chromosomes.[77] These specialized chromosome caps also help protect the DNA ends, and stop the DNA repair systems in the cell from treating them as damage to be corrected.[78] In human cells, telomeres are usually lengths of single-stranded DNA containing several thousand repeats of a simple TTAGGG sequence.[79]

text: These guanine-rich sequences may stabilize chromosome ends by forming structures of stacked sets of four-base units, rather than the usual base pairs found in other DNA molecules. Here, four guanine bases form a flat plate and these flat four-base units then stack on top of each other, to form a stable G-quadruplex structure.[81] These structures are stabilized by hydrogen bonding between the edges of the bases and chelation of a metal ion in the centre of each four-base unit.[82] Other structures can also be formed, with the central set of four bases coming from either a single strand folded around the bases, or several different parallel strands, each contributing one base to the central structure.

text: In addition to these stacked structures, telomeres also form large loop structures called telomere loops, or T-loops. Here, the single-stranded DNA curls around in a long circle stabilized by telomere-binding proteins.[83] At the very end of the T-loop, the single-stranded telomere DNA is held onto a region of double-stranded DNA by the telomere strand disrupting the double-helical DNA and base pairing to one of the two strands. This triple-stranded structure is called a displacement loop or D-loop.[81]

text:
Single branch
Multiple branches

text: Branched DNA

text: In DNA, fraying occurs when non-complementary regions exist at the end of an otherwise complementary double-strand of DNA. However, branched DNA can occur if a third strand of DNA is introduced and contains adjoining regions able to hybridize with the frayed regions of the pre-existing double-strand. Although the simplest example of branched DNA involves only three strands of DNA, complexes involving additional strands and multiple branches are also possible.[84] Branched DNA can be used in nanotechnology to construct geometric shapes, see the section on uses in technology below.

text: Chemical modifications and altered DNA packaging

text:
cytosine
5-methylcytosine
thymine

text: Base modifications and DNA packaging

text: The expression of genes is influenced by how the DNA is packaged in chromosomes, in a structure called chromatin. Base modifications can be involved in packaging, with regions that have low or no gene expression usually containing high levels of methylation of cytosine bases. DNA packaging and its influence on gene expression can also occur by covalent modifications of the histone protein core around which DNA is wrapped in the chromatin structure or else by remodeling carried out by chromatin remodeling complexes (see Chromatin remodeling). There is, further, crosstalk between DNA methylation and histone modification, so they can coordinately affect chromatin and gene expression.[85]

text: For one example, cytosine methylation produces 5-methylcytosine, which is important for X-inactivation of chromosomes.[86] The average level of methylation varies between organisms – the worm Caenorhabditis elegans lacks cytosine methylation, while vertebrates have higher levels, with up to 1% of their DNA containing 5-methylcytosine.[87] Despite the importance of 5-methylcytosine, it can deaminate to leave a thymine base, so methylated cytosines are particularly prone to mutations.[88] Other base modifications include adenine methylation in bacteria, the presence of 5-hydroxymethylcytosine in the brain,[89] and the glycosylation of uracil to produce the "J-base" in kinetoplastids.[90][91]

text: Damage

text: DNA can be damaged by many sorts of mutagens, which change the DNA sequence. Mutagens include oxidizing agents, alkylating agents and also high-energy electromagnetic radiation such as ultraviolet light and X-rays. The type of DNA damage produced depends on the type of mutagen. For example, UV light can damage DNA by producing thymine dimers, which are cross-links between pyrimidine bases.[93] On the other hand, oxidants such as free radicals or hydrogen peroxide produce multiple forms of damage, including base modifications, particularly of guanosine, and double-strand breaks.[94] A typical human cell contains about 150,000 bases that have suffered oxidative damage.[95] Of these oxidative lesions, the most dangerous are double-strand breaks, as these are difficult to repair and can produce point mutations, insertions, deletions from the DNA sequence, and chromosomal translocations.[96] These mutations can cause cancer. Because of inherent limits in the DNA repair mechanisms, if humans lived long enough, they would all eventually develop cancer.[97][98] DNA damages that are naturally occurring, due to normal cellular processes that produce reactive oxygen species, the hydrolytic activities of cellular water, etc., also occur frequently. Although most of these damages are repaired, in any cell some DNA damage may remain despite the action of repair processes. These remaining DNA damages accumulate with age in mammalian postmitotic tissues. This accumulation appears to be an important underlying cause of aging.[99][100][101]

text: Many mutagens fit into the space between two adjacent base pairs, this is called intercalation. Most intercalators are aromatic and planar molecules; examples include ethidium bromide, acridines, daunomycin, and doxorubicin. For an intercalator to fit between base pairs, the bases must separate, distorting the DNA strands by unwinding of the double helix. This inhibits both transcription and DNA replication, causing toxicity and mutations.[102] As a result, DNA intercalators may be carcinogens, and in the case of thalidomide, a teratogen.[103] Others such as benzo[a]pyrene diol epoxide and aflatoxin form DNA adducts that induce errors in replication.[104] Nevertheless, due to their ability to inhibit DNA transcription and replication, other similar toxins are also used in chemotherapy to inhibit rapidly growing cancer cells.[105]

text: Biological functions

text: DNA usually occurs as linear chromosomes in eukaryotes, and circular chromosomes in prokaryotes. The set of chromosomes in a cell makes up its genome; the human genome has approximately 3 billion base pairs of DNA arranged into 46 chromosomes.[106] The information carried by DNA is held in the sequence of pieces of DNA called genes. Transmission of genetic information in genes is achieved via complementary base pairing. For example, in transcription, when a cell uses the information in a gene, the DNA sequence is copied into a complementary RNA sequence through the attraction between the DNA and the correct RNA nucleotides. Usually, this RNA copy is then used to make a matching protein sequence in a process called translation, which depends on the same interaction between RNA nucleotides. In alternative fashion, a cell may simply copy its genetic information in a process called DNA replication. The details of these functions are covered in other articles; here the focus is on the interactions between DNA and other molecules that mediate the function of the genome.

text: Genes and genomes

text: Genomic DNA is tightly and orderly packed in the process called DNA condensation, to fit the small available volumes of the cell. In eukaryotes, DNA is located in the cell nucleus, with small amounts in mitochondria and chloroplasts. In prokaryotes, the DNA is held within an irregularly shaped body in the cytoplasm called the nucleoid.[107] The genetic information in a genome is held within genes, and the complete set of this information in an organism is called its genotype. A gene is a unit of heredity and is a region of DNA that influences a particular characteristic in an organism. Genes contain an open reading frame that can be transcribed, and regulatory sequences such as promoters and enhancers, which control transcription of the open reading frame.

text: In many species, only a small fraction of the total sequence of the genome encodes protein. For example, only about 1.5% of the human genome consists of protein-coding exons, with over 50% of human DNA consisting of non-coding repetitive sequences.[108] The reasons for the presence of so much noncoding DNA in eukaryotic genomes and the extraordinary differences in genome size, or C-value, among species, represent a long-standing puzzle known as the "C-value enigma".[109] However, some DNA sequences that do not code protein may still encode functional non-coding RNA molecules, which are involved in the regulation of gene expression.[110]

text: Some noncoding DNA sequences play structural roles in chromosomes. Telomeres and centromeres typically contain few genes but are important for the function and stability of chromosomes.[78][112] An abundant form of noncoding DNA in humans are pseudogenes, which are copies of genes that have been disabled by mutation.[113] These sequences are usually just molecular fossils, although they can occasionally serve as raw genetic material for the creation of new genes through the process of gene duplication and divergence.[114]

text: Transcription and translation

text: A gene is a sequence of DNA that contains genetic information and can influence the phenotype of an organism. Within a gene, the sequence of bases along a DNA strand defines a messenger RNA sequence, which then defines one or more protein sequences. The relationship between the nucleotide sequences of genes and the amino-acid sequences of proteins is determined by the rules of translation, known collectively as the genetic code. The genetic code consists of three-letter 'words' called codons formed from a sequence of three nucleotides (e.g. ACT, CAG, TTT).

text: In transcription, the codons of a gene are copied into messenger RNA by RNA polymerase. This RNA copy is then decoded by a ribosome that reads the RNA sequence by base-pairing the messenger RNA to transfer RNA, which carries amino acids. Since there are 4 bases in 3-letter combinations, there are 64 possible codons (43 combinations). These encode the twenty standard amino acids, giving most amino acids more than one possible codon. There are also three 'stop' or 'nonsense' codons signifying the end of the coding region; these are the TAA, TGA, and TAG codons.

text: Replication

text: Cell division is essential for an organism to grow, but, when a cell divides, it must replicate the DNA in its genome so that the two daughter cells have the same genetic information as their parent. The double-stranded structure of DNA provides a simple mechanism for DNA replication. Here, the two strands are separated and then each strand's complementary DNA sequence is recreated by an enzyme called DNA polymerase. This enzyme makes the complementary strand by finding the correct base through complementary base pairing and bonding it onto the original strand. As DNA polymerases can only extend a DNA strand in a 5′ to 3′ direction, different mechanisms are used to copy the antiparallel strands of the double helix.[115] In this way, the base on the old strand dictates which base appears on the new strand, and the cell ends up with a perfect copy of its DNA.

text: Extracellular nucleic acids

text: Naked extracellular DNA (eDNA), most of it released by cell death, is nearly ubiquitous in the environment. Its concentration in soil may be as high as 2 μg/L, and its concentration in natural aquatic environments may be as high at 88 μg/L.[116] Various possible functions have been proposed for eDNA: it may be involved in horizontal gene transfer;[117] it may provide nutrients;[118] and it may act as a buffer to recruit or titrate ions or antibiotics.[119] Extracellular DNA acts as a functional extracellular matrix component in the biofilms of several bacterial species. It may act as a recognition factor to regulate the attachment and dispersal of specific cell types in the biofilm;[120] it may contribute to biofilm formation;[121] and it may contribute to the biofilm's physical strength and resistance to biological stress.[122]

text: Cell-free fetal DNA is found in the blood of the mother, and can be sequenced to determine a great deal of information about the developing fetus.[123]

text: Interactions with proteins

text: All the functions of DNA depend on interactions with proteins. These protein interactions can be non-specific, or the protein can bind specifically to a single DNA sequence. Enzymes can also bind to DNA and of these, the polymerases that copy the DNA base sequence in transcription and DNA replication are particularly important.

text: DNA-binding proteins

text: Structural proteins that bind DNA are well-understood examples of non-specific DNA-protein interactions. Within chromosomes, DNA is held in complexes with structural proteins. These proteins organize the DNA into a compact structure called chromatin. In eukaryotes, this structure involves DNA binding to a complex of small basic proteins called histones, while in prokaryotes multiple types of proteins are involved.[124][125] The histones form a disk-shaped complex called a nucleosome, which contains two complete turns of double-stranded DNA wrapped around its surface. These non-specific interactions are formed through basic residues in the histones, making ionic bonds to the acidic sugar-phosphate backbone of the DNA, and are thus largely independent of the base sequence.[126] Chemical modifications of these basic amino acid residues include methylation, phosphorylation, and acetylation.[127] These chemical changes alter the strength of the interaction between the DNA and the histones, making the DNA more or less accessible to transcription factors and changing the rate of transcription.[128] Other non-specific DNA-binding proteins in chromatin include the high-mobility group proteins, which bind to bent or distorted DNA.[129] These proteins are important in bending arrays of nucleosomes and arranging them into the larger structures that make up chromosomes.[130]

text: A distinct group of DNA-binding proteins is the DNA-binding proteins that specifically bind single-stranded DNA. In humans, replication protein A is the best-understood member of this family and is used in processes where the double helix is separated, including DNA replication, recombination, and DNA repair.[131] These binding proteins seem to stabilize single-stranded DNA and protect it from forming stem-loops or being degraded by nucleases.

text: In contrast, other proteins have evolved to bind to particular DNA sequences. The most intensively studied of these are the various transcription factors, which are proteins that regulate transcription. Each transcription factor binds to one particular set of DNA sequences and activates or inhibits the transcription of genes that have these sequences close to their promoters. The transcription factors do this in two ways. Firstly, they can bind the RNA polymerase responsible for transcription, either directly or through other mediator proteins; this locates the polymerase at the promoter and allows it to begin transcription.[133] Alternatively, transcription factors can bind enzymes that modify the histones at the promoter. This changes the accessibility of the DNA template to the polymerase.[134]

text: As these DNA targets can occur throughout an organism's genome, changes in the activity of one type of transcription factor can affect thousands of genes.[135] Consequently, these proteins are often the targets of the signal transduction processes that control responses to environmental changes or cellular differentiation and development. The specificity of these transcription factors' interactions with DNA come from the proteins making multiple contacts to the edges of the DNA bases, allowing them to "read" the DNA sequence. Most of these base-interactions are made in the major groove, where the bases are most accessible.[46]

text: DNA-modifying enzymes

text: Nucleases and ligases

text: Nucleases are enzymes that cut DNA strands by catalyzing the hydrolysis of the phosphodiester bonds. Nucleases that hydrolyse nucleotides from the ends of DNA strands are called exonucleases, while endonucleases cut within strands. The most frequently used nucleases in molecular biology are the restriction endonucleases, which cut DNA at specific sequences. For instance, the EcoRV enzyme shown to the left recognizes the 6-base sequence 5′-GATATC-3′ and makes a cut at the horizontal line. In nature, these enzymes protect bacteria against phage infection by digesting the phage DNA when it enters the bacterial cell, acting as part of the restriction modification system.[137] In technology, these sequence-specific nucleases are used in molecular cloning and DNA fingerprinting.

text: Enzymes called DNA ligases can rejoin cut or broken DNA strands.[138] Ligases are particularly important in lagging strand DNA replication, as they join together the short segments of DNA produced at the replication fork into a complete copy of the DNA template. They are also used in DNA repair and genetic recombination.[138]

text: Topoisomerases and helicases

text: Topoisomerases are enzymes with both nuclease and ligase activity. These proteins change the amount of supercoiling in DNA. Some of these enzymes work by cutting the DNA helix and allowing one section to rotate, thereby reducing its level of supercoiling; the enzyme then seals the DNA break.[59] Other types of these enzymes are capable of cutting one DNA helix and then passing a second strand of DNA through this break, before rejoining the helix.[139] Topoisomerases are required for many processes involving DNA, such as DNA replication and transcription.[60]

text: Helicases are proteins that are a type of molecular motor. They use the chemical energy in nucleoside triphosphates, predominantly adenosine triphosphate (ATP), to break hydrogen bonds between bases and unwind the DNA double helix into single strands.[140] These enzymes are essential for most processes where enzymes need to access the DNA bases.

text: Polymerases

text: Polymerases are enzymes that synthesize polynucleotide chains from nucleoside triphosphates. The sequence of their products is created based on existing polynucleotide chains—which are called templates. These enzymes function by repeatedly adding a nucleotide to the 3′ hydroxyl group at the end of the growing polynucleotide chain. As a consequence, all polymerases work in a 5′ to 3′ direction.[141] In the active site of these enzymes, the incoming nucleoside triphosphate base-pairs to the template: this allows polymerases to accurately synthesize the complementary strand of their template. Polymerases are classified according to the type of template that they use.

text: In DNA replication, DNA-dependent DNA polymerases make copies of DNA polynucleotide chains. To preserve biological information, it is essential that the sequence of bases in each copy are precisely complementary to the sequence of bases in the template strand. Many DNA polymerases have a proofreading activity. Here, the polymerase recognizes the occasional mistakes in the synthesis reaction by the lack of base pairing between the mismatched nucleotides. If a mismatch is detected, a 3′ to 5′ exonuclease activity is activated and the incorrect base removed.[142] In most organisms, DNA polymerases function in a large complex called the replisome that contains multiple accessory subunits, such as the DNA clamp or helicases.[143]

text: RNA-dependent DNA polymerases are a specialized class of polymerases that copy the sequence of an RNA strand into DNA. They include reverse transcriptase, which is a viral enzyme involved in the infection of cells by retroviruses, and telomerase, which is required for the replication of telomeres.[77][144] For example, HIV reverse transcriptase is an enzyme for AIDS virus replication.[144] Telomerase is an unusual polymerase because it contains its own RNA template as part of its structure. It synthesizes telomeres at the ends of chromosomes. Telomeres prevent fusion of the ends of neighboring chromosomes and protect chromosome ends from damage.[78]

text: Transcription is carried out by a DNA-dependent RNA polymerase that copies the sequence of a DNA strand into RNA. To begin transcribing a gene, the RNA polymerase binds to a sequence of DNA called a promoter and separates the DNA strands. It then copies the gene sequence into a messenger RNA transcript until it reaches a region of DNA called the terminator, where it halts and detaches from the DNA. As with human DNA-dependent DNA polymerases, RNA polymerase II, the enzyme that transcribes most of the genes in the human genome, operates as part of a large protein complex with multiple regulatory and accessory subunits.[145]

text: Genetic recombination

text: A DNA helix usually does not interact with other segments of DNA, and in human cells, the different chromosomes even occupy separate areas in the nucleus called "chromosome territories".[147] This physical separation of different chromosomes is important for the ability of DNA to function as a stable repository for information, as one of the few times chromosomes interact is in chromosomal crossover which occurs during sexual reproduction, when genetic recombination occurs. Chromosomal crossover is when two DNA helices break, swap a section and then rejoin.

text: Recombination allows chromosomes to exchange genetic information and produces new combinations of genes, which increases the efficiency of natural selection and can be important in the rapid evolution of new proteins.[148] Genetic recombination can also be involved in DNA repair, particularly in the cell's response to double-strand breaks.[149]

text: The most common form of chromosomal crossover is homologous recombination, where the two chromosomes involved share very similar sequences. Non-homologous recombination can be damaging to cells, as it can produce chromosomal translocations and genetic abnormalities. The recombination reaction is catalyzed by enzymes known as recombinases, such as RAD51.[150] The first step in recombination is a double-stranded break caused by either an endonuclease or damage to the DNA.[151] A series of steps catalyzed in part by the recombinase then leads to joining of the two helices by at least one Holliday junction, in which a segment of a single strand in each helix is annealed to the complementary strand in the other helix. The Holliday junction is a tetrahedral junction structure that can be moved along the pair of chromosomes, swapping one strand for another. The recombination reaction is then halted by cleavage of the junction and re-ligation of the released DNA.[152] Only strands of like polarity exchange DNA during recombination. There are two types of cleavage: east-west cleavage and north-south cleavage. The north-south cleavage nicks both strands of DNA, while the east-west cleavage has one strand of DNA intact. The formation of a Holliday junction during recombination makes it possible for genetic diversity, genes to exchange on chromosomes, and expression of wild-type viral genomes.

text: Evolution

text: DNA contains the genetic information that allows all modern living things to function, grow and reproduce. However, it is unclear how long in the 4-billion-year history of life DNA has performed this function, as it has been proposed that the earliest forms of life may have used RNA as their genetic material.[153][154] RNA may have acted as the central part of early cell metabolism as it can both transmit genetic information and carry out catalysis as part of ribozymes.[155] This ancient RNA world where nucleic acid would have been used for both catalysis and genetics may have influenced the evolution of the current genetic code based on four nucleotide bases. This would occur, since the number of different bases in such an organism is a trade-off between a small number of bases increasing replication accuracy and a large number of bases increasing the catalytic efficiency of ribozymes.[156] However, there is no direct evidence of ancient genetic systems, as recovery of DNA from most fossils is impossible because DNA survives in the environment for less than one million years, and slowly degrades into short fragments in solution.[157] Claims for older DNA have been made, most notably a report of the isolation of a viable bacterium from a salt crystal 250 million years old,[158] but these claims are controversial.[159][160]

text: Building blocks of DNA (adenine, guanine, and related organic molecules) may have been formed extraterrestrially in outer space.[161][162][163] Complex DNA and RNA organic compounds of life, including uracil, cytosine, and thymine, have also been formed in the laboratory under conditions mimicking those found in outer space, using starting chemicals, such as pyrimidine, found in meteorites. Pyrimidine, like polycyclic aromatic hydrocarbons (PAHs), the most carbon-rich chemical found in the universe, may have been formed in red giants or in interstellar cosmic dust and gas clouds.[164]

text: Uses in technology

text: Genetic engineering

text: Methods have been developed to purify DNA from organisms, such as phenol-chloroform extraction, and to manipulate it in the laboratory, such as restriction digests and the polymerase chain reaction. Modern biology and biochemistry make intensive use of these techniques in recombinant DNA technology. Recombinant DNA is a man-made DNA sequence that has been assembled from other DNA sequences. They can be transformed into organisms in the form of plasmids or in the appropriate format, by using a viral vector.[165] The genetically modified organisms produced can be used to produce products such as recombinant proteins, used in medical research,[166] or be grown in agriculture.[167][168]

text: DNA profiling

text: Forensic scientists can use DNA in blood, semen, skin, saliva or hair found at a crime scene to identify a matching DNA of an individual, such as a perpetrator.[169] This process is formally termed DNA profiling, but may also be called "genetic fingerprinting". In DNA profiling, the lengths of variable sections of repetitive DNA, such as short tandem repeats and minisatellites, are compared between people. This method is usually an extremely reliable technique for identifying a matching DNA.[170] However, identification can be complicated if the scene is contaminated with DNA from several people.[171] DNA profiling was developed in 1984 by British geneticist Sir Alec Jeffreys,[172] and first used in forensic science to convict Colin Pitchfork in the 1988 Enderby murders case.[173]

text: The development of forensic science and the ability to now obtain genetic matching on minute samples of blood, skin, saliva, or hair has led to re-examining many cases. Evidence can now be uncovered that was scientifically impossible at the time of the original examination. Combined with the removal of the double jeopardy law in some places, this can allow cases to be reopened where prior trials have failed to produce sufficient evidence to convince a jury. People charged with serious crimes may be required to provide a sample of DNA for matching purposes. The most obvious defense to DNA matches obtained forensically is to claim that cross-contamination of evidence has occurred. This has resulted in meticulous strict handling procedures with new cases of serious crime. DNA profiling is also used successfully to positively identify victims of mass casualty incidents,[174] bodies or body parts in serious accidents, and individual victims in mass war graves, via matching to family members.

text: DNA profiling is also used in DNA paternity testing to determine if someone is the biological parent or grandparent of a child with the probability of parentage is typically 99.99% when the alleged parent is biologically related to the child. Normal DNA sequencing methods happen after birth, but there are new methods to test paternity while a mother is still pregnant.[175]

text: DNA enzymes or catalytic DNA

text: Deoxyribozymes, also called DNAzymes or catalytic DNA, are first discovered in 1994.[176] They are mostly single stranded DNA sequences isolated from a large pool of random DNA sequences through a combinatorial approach called in vitro selection or systematic evolution of ligands by exponential enrichment (SELEX). DNAzymes catalyze variety of chemical reactions including RNA-DNA cleavage, RNA-DNA ligation, amino acids phosphorylation-dephosphorylation, carbon-carbon bond formation, and etc. DNAzymes can enhance catalytic rate of chemical reactions up to 100,000,000,000-fold over the uncatalyzed reaction.[177] The most extensively studied class of DNAzymes is RNA-cleaving types which have been used to detect different metal ions and designing therapeutic agents. Several metal-specific DNAzymes have been reported including the GR-5 DNAzyme (lead-specific),[176] the CA1-3 DNAzymes (copper-specific),[178] the 39E DNAzyme (uranyl-specific) and the NaA43 DNAzyme (sodium-specific).[179] The NaA43 DNAzyme, which is reported to be more than 10,000-fold selective for sodium over other metal ions, was used to make a real-time sodium sensor in living cells.

text: Bioinformatics

text: Bioinformatics involves the development of techniques to store, data mine, search and manipulate biological data, including DNA nucleic acid sequence data. These have led to widely applied advances in computer science, especially string searching algorithms, machine learning, and database theory.[180] String searching or matching algorithms, which find an occurrence of a sequence of letters inside a larger sequence of letters, were developed to search for specific sequences of nucleotides.[181] The DNA sequence may be aligned with other DNA sequences to identify homologous sequences and locate the specific mutations that make them distinct. These techniques, especially multiple sequence alignment, are used in studying phylogenetic relationships and protein function.[182] Data sets representing entire genomes' worth of DNA sequences, such as those produced by the Human Genome Project, are difficult to use without the annotations that identify the locations of genes and regulatory elements on each chromosome. Regions of DNA sequence that have the characteristic patterns associated with protein- or RNA-coding genes can be identified by gene finding algorithms, which allow researchers to predict the presence of particular gene products and their possible functions in an organism even before they have been isolated experimentally.[183] Entire genomes may also be compared, which can shed light on the evolutionary history of particular organism and permit the examination of complex evolutionary events.

text: DNA nanotechnology

text: DNA nanotechnology uses the unique molecular recognition properties of DNA and other nucleic acids to create self-assembling branched DNA complexes with useful properties.[184] DNA is thus used as a structural material rather than as a carrier of biological information. This has led to the creation of two-dimensional periodic lattices (both tile-based and using the DNA origami method) and three-dimensional structures in the shapes of polyhedra.[185] Nanomechanical devices and algorithmic self-assembly have also been demonstrated,[186] and these DNA structures have been used to template the arrangement of other molecules such as gold nanoparticles and streptavidin proteins.[187]

text: History and anthropology

text: Because DNA collects mutations over time, which are then inherited, it contains historical information, and, by comparing DNA sequences, geneticists can infer the evolutionary history of organisms, their phylogeny.[188] This field of phylogenetics is a powerful tool in evolutionary biology. If DNA sequences within a species are compared, population geneticists can learn the history of particular populations. This can be used in studies ranging from ecological genetics to anthropology; For example, DNA evidence is being used to try to identify the Ten Lost Tribes of Israel.[189][190]

text: Information storage

text: In a paper published in Nature in January 2013, scientists from the European Bioinformatics Institute and Agilent Technologies proposed a mechanism to use DNA's ability to code information as a means of digital data storage. The group was able to encode 739 kilobytes of data into DNA code, synthesize the actual DNA, then sequence the DNA and decode the information back to its original form, with a reported 100% accuracy. The encoded information consisted of text files and audio files. A prior experiment was published in August 2012. It was conducted by researchers at Harvard University, where the text of a 54,000-word book was encoded in DNA.[191][192]

text: Moreover, in living cells, the storage can be turned active by enzymes. Light-gated protein domains fused to DNA processing enzymes are suitable for that task in vitro.[193][194] Fluorescent exonucleases can transmit the output according to the nucleotide they have read.[195]

text: History

text: DNA was first isolated by the Swiss physician Friedrich Miescher who, in 1869, discovered a microscopic substance in the pus of discarded surgical bandages. As it resided in the nuclei of cells, he called it "nuclein".[196][197] In 1878, Albrecht Kossel isolated the non-protein component of "nuclein", nucleic acid, and later isolated its five primary nucleobases.[198][199]

text: In 1909, Phoebus Levene identified the base, sugar, and phosphate nucleotide unit of the RNA (then named "yeast nucleic acid").[200][201][202] In 1929, Levene identified deoxyribose sugar in "thymus nucleic acid" (DNA).[203] Levene suggested that DNA consisted of a string of four nucleotide units linked together through the phosphate groups ("tetranucleotide hypothesis"). Levene thought the chain was short and the bases repeated in a fixed order. In 1927, Nikolai Koltsov proposed that inherited traits would be inherited via a "giant hereditary molecule" made up of "two mirror strands that would replicate in a semi-conservative fashion using each strand as a template".[204][205] In 1928, Frederick Griffith in his experiment discovered that traits of the "smooth" form of Pneumococcus could be transferred to the "rough" form of the same bacteria by mixing killed "smooth" bacteria with the live "rough" form.[206][207] This system provided the first clear suggestion that DNA carries genetic information.

text: In 1933, while studying virgin sea urchin eggs, Jean Brachet suggested that DNA is found in cell nucleus and that RNA is present exclusively in the cytoplasm. At the time, "yeast nucleic acid" (RNA) was thought to occur only in plants, while "thymus nucleic acid" (DNA) only in animals. The latter was thought to be a tetramer, with the function of buffering cellular pH.[208][209]

text: In 1937, William Astbury produced the first X-ray diffraction patterns that showed that DNA had a regular structure.[210]

text: In 1943, Oswald Avery, along with coworkers Colin MacLeod and Maclyn McCarty, identified DNA as the transforming principle, supporting Griffith's suggestion (Avery–MacLeod–McCarty experiment).[211] DNA's role in heredity was confirmed in 1952 when Alfred Hershey and Martha Chase in the Hershey–Chase experiment showed that DNA is the genetic material of the T2 phage.[212]

text: Late in 1951, Francis Crick started working with James Watson at the Cavendish Laboratory within the University of Cambridge. In 1953, Watson and Crick suggested what is now accepted as the first correct double-helix model of DNA structure in the journal Nature.[9] Their double-helix, molecular model of DNA was then based on one X-ray diffraction image (labeled as "Photo 51")[213] taken by Rosalind Franklin and Raymond Gosling in May 1952, and the information that the DNA bases are paired. On 28 February 1953 Crick interrupted patrons' lunchtime at The Eagle pub in Cambridge to announce that he and Watson had "discovered the secret of life".[214]

text: Months earlier, in February 1953, Linus Pauling and Robert Corey proposed a model for nucleic acids containing three intertwined chains, with the phosphates near the axis, and the bases on the outside.[215] Experimental evidence supporting the Watson and Crick model was published in a series of five articles in the same issue of Nature.[216] Of these, Franklin and Gosling's paper was the first publication of their own X-ray diffraction data and original analysis method that partly supported the Watson and Crick model;[63][217] this issue also contained an article on DNA structure by Maurice Wilkins and two of his colleagues, whose analysis and in vivo B-DNA X-ray patterns also supported the presence in vivo of the double-helical DNA configurations as proposed by Crick and Watson for their double-helix molecular model of DNA in the prior two pages of Nature.[64] In 1962, after Franklin's death, Watson, Crick, and Wilkins jointly received the Nobel Prize in Physiology or Medicine.[218] Nobel Prizes are awarded only to living recipients. A debate continues about who should receive credit for the discovery.[219]

text: In an influential presentation in 1957, Crick laid out the central dogma of molecular biology, which foretold the relationship between DNA, RNA, and proteins, and articulated the "adaptor hypothesis".[220] Final confirmation of the replication mechanism that was implied by the double-helical structure followed in 1958 through the Meselson–Stahl experiment.[221] Further work by Crick and coworkers showed that the genetic code was based on non-overlapping triplets of bases, called codons, allowing Har Gobind Khorana, Robert W. Holley, and Marshall Warren Nirenberg to decipher the genetic code.[222] These findings represent the birth of molecular biology.[223]


document_title: Shot clock

question_text: when did the nba institute the shot clock

text: Shot clock

text: History[edit]

text: Background[edit]

text: The NBA (National Basketball Association) had problems attracting fans (and positive media coverage) before the shot clock's inception.[2] This was due to teams running out the clock once they were leading in a game; without the shot clock, teams passed the ball nearly endlessly without penalty. If one team chose to stall, the other team (especially if behind) would often commit fouls to get the ball back following the free throw. Very low-scoring games with many fouls were common, which bored fans. The most extreme case occurred on November 22, 1950, when the Fort Wayne Pistons defeated the Minneapolis Lakers by a record-low score of 19–18, including 3–1 in the fourth quarter.[3] The Pistons held the ball for minutes at a time without shooting (they attempted 13 shots for the game) in order to limit the impact of the Lakers' dominant George Mikan. The Pistons' performance led the St. Paul Dispatch to write "[The Pistons] gave pro basketball a great black eye."[4] NBA President Maurice Podoloff said, "In our game, with the number of stars we have, we of necessity run up big scores."[5] A few weeks after the Pistons/Lakers game, the Rochester Royals and Indianapolis Olympians played a six-overtime game with only one shot in each overtime - in each overtime period, the team who had the ball first held the ball for the entirety of the period before attempting a last-second shot. The NBA tried several rule changes in the early 1950s to speed up the game and reduce fouls before eventually adopting the shot clock.

text: Creation[edit]

text: The shot clock first came to use in 1954 in Syracuse, New York, where Syracuse Nationals (now the Philadelphia 76ers) owner Danny Biasone and general manager Leo Ferris experimented using a 24-second version during a scrimmage game.[6] According to Biasone, "I looked at the box scores from the games I enjoyed, games where they didn't screw around and stall. I noticed each team took about 60 shots. That meant 120 shots per game. So I took 2,880 seconds (48 minutes) and divided that by 120 shots. The result was 24 seconds per shot."[3][7] Biasone and Ferris then convinced the NBA to adopt it for the 1954–55 season, a season in which the Nationals won the NBA Championship.

text: Syracuse Nationals General Manager Leo Ferris has emerged in the discussion as one of those involved in the creation and development of the shot clock. Along with Danny Biasone and Emil Barboni, a scout for the Nats, Leo Ferris was a key figure in developing the 24-second clock.[8] Jack Andrews, longtime basketball writer for The Syracuse Post-Standard, often recalled how Ferris would sit at Danny Biasone's Eastwood bowling alley, scribbling potential shot clock formulas onto a napkin.[9] Ferris, who loved mathematics, ended up dividing the number of seconds in a 48-minute game (2,880) by the average number of shots taken in a game (120) to get to the 24-second time limit per possession.[10] While he and Biasone often share in the credit for the shot clock, it was Ferris who was singled out by business manager Bob Sexton at the 1954 team banquet for pushing the shot clock rule.

text: Use and reaction[edit]

text: When it was first introduced by the NBA, the 24-second shot clock made players so nervous that it hardly came into play, as players were taking fewer than 20 seconds to shoot. According to Syracuse star Dolph Schayes, "We thought we had to take quick shots – a pass and a shot was it – maybe 8–10 seconds... But as the game went on, we saw the inherent genius in Danny's 24 seconds – you could work the ball around [the offensive zone] for a good shot."[7]

text: The shot clock, together with some rule changes concerning fouls, revolutionized NBA basketball. In the last pre-clock season (1953–54), teams averaged 79 points per game; in the first year with the clock (1954–55), the average was 93 points,[3] which went up to 107 points by its fourth year in use (1957–58).[11] The advent of the shot clock (and the resulting increase in scoring) coincided with an increase in attendance, which increased 40% within a few years to an average of 4,800 per game.[12]

text: The shot clock received near-universal praise for its role in improving the style of play in the NBA. Coach and referee Charley Eckman said, "Danny Biasone saved the NBA with the 24-second rule."[13] Boston Celtic all-star Bob Cousy said, "Before the new rule, the last quarter could be deadly. The team in front would hold the ball indefinitely, and the only way you could get it was by fouling somebody. In the meantime, nobody dared take a shot and the whole game slowed up. With the clock, we have constant action. I think it saved the NBA at that time. It allowed the game to breathe and progress."[14] League president Maurice Podoloff called the adoption of the shot clock "the most important event in the NBA."[3] The league itself states, "Biasone's invention rescue[d] the league."[13]

text: Adoption by other leagues[edit]

text: Two later pro leagues that rivaled the NBA adopted a modified version of the shot clock. The American Basketball League used a 30-second shot clock for its two years in existence (1961–1963). The American Basketball Association also adopted a 30-second clock when it launched in 1967–68, switching to the NBA's 24-second length for its final season (1975–76).

text: In the 1969–70 season, women's collegiate basketball (at the time sanctioned by the Commission on Intercollegiate Athletics for Women) used a 30-second shot clock on an experimental basis, officially adopting it for the 1970–71 season.[15] Unlike the women's side, there was initial resistance to the implementation of a shot clock for men's NCAA basketball, due to fears that smaller colleges would be unable to compete with powerhouses in a running game. However, after extreme results like an 11–6 Tennessee win over Temple in 1973, support for a men's shot clock began to build.[16] The NCAA introduced a 45-second shot clock for the men's game in the 1985–86 season, reducing it to 35 seconds in the 1993–94 season[17] and 30 seconds in the 2015–16 season.[18] The NAIA also reduced the shot clock to 30 seconds for men's basketball starting in 2015–16.[19]

text: From its inception in 1975, the Philippine Basketball Association adopted a 25-second shot clock. This was because the shot clocks then installed at the league's main venues, the Araneta Coliseum and Rizal Memorial Coliseum (the latter no longer used by the league), could only be set at 5-second intervals. The league later adopted a 24-second clock starting from the 1995 season. The Metropolitan Basketball Association in the Philippines used the 23-second clock from its maiden season in 1998. In Filipino college basketball, the NCAA Basketball Championship (Philippines) and the UAAP Basketball Championship adopted a 30-second clock; they switched to 24 seconds starting with the 2001–02 season, the first season to start after the FIBA rule change in 2001.

text: Operation[edit]

text: In the NBA (since 1954), Women's National Basketball Association (since 2006), and FIBA play (since 2000; 30-second from 1956 to 2000), the shot clock counts down 24 seconds, thus often being called the "24-second clock." If a shot is attempted and hits or enters the rim, or if the defensive team gains possession via a rebound, steal, or out-of-bounds play, the shot clock resets. Failure by the offense to attempt a shot that hits the rim within the prescribed time results in a "shot clock violation" and a loss of possession to the other team. Three signals indicate when the shot clock expires—a shot clock signal, illuminated lights on the shot clock (NBA, FIBA, Euroleague, and many venues using an NBA-style transparent shot clock), and in the (W)NBA and FIBA play (starting in July 2018), a yellow LED light strip on the backboard. In the 2011–12 NBA season and 2014–15 Euroleague, the last five seconds of the shot clock were modified to include tenths of a second, allowing offensive players to see precisely how much time they have to shoot and officials to determine any last-second shots easily. The rule has been adopted by FIBA starting in 2018.[20] In the 2016-17 NBA season, a new 'official timekeeper' deal for the NBA with Swiss watch manufacturer Tissot introduced a new united official game clock/shot clock system, putting both timing systems under the same system for the first time.[21] Tissot also became official timekeeper for the WNBA in the 2017 season.

text: Furthermore, the shot clock is not reset on a foul in the frontcourt. Rule changes in the NBA since 1998, and in FIBA after 2010 state the shot clock will be reset only if 13 seconds or fewer are on the shot clock, after which it is reset to 14 seconds.

text: The (W)NBA and Euroleague have different rules on the shot clock reset on jump balls; while both leagues have jump balls retained by the offense are reset to 14 seconds (if 13 seconds or fewer are on the shot clock), in the (W)NBA, if the defence causes the jump ball, the shot clock is not reset if the offense keeps control of the ball unless under 5.0 seconds of time remain, where it is reset to 5.0 seconds.

text: Also in FIBA play, if the offense retains control of a ball following a rebound, the shot clock is reset to 14 seconds.

text: Since the 2015–16 season, all American college basketball uses a 30-second shot clock, while Canadian university basketball uses a 24-second clock. The American women's game has used a 30-second clock since the 1970s, but the men's game did not adopt a shot clock until 1985. The men's limit was originally 45 seconds, and was shortened to 35 seconds in 1993 before going to 30 seconds in 2015. The National Federation of State High School Associations (NFHS), which sets rules for high school basketball in the U.S., does not mandate the use of a shot clock, instead leaving the choice to use a clock and its duration up to each individual state association. Proposals to adopt a national shot clock for high school basketball have been voted down by the NFHS as recently as 2011.[22] Currently, eight U.S. states require the use of a shot clock of 30/35 seconds in high school competition: California, Maryland, Massachusetts, New York, North Dakota, Rhode Island, South Dakota, and Washington.[22]

text:
Organization
Duration

NBA
24 seconds
14 seconds (offensive retains control after fouls)

WNBA

U Sports (Canadian universities)

NCAA, NAIA
30 seconds

United States high school basketball
30/35 seconds (some states only)

FIBA
24 seconds (full-court game)
14 seconds (reset when offense retains ball)
12 seconds (3x3 half-court)[23]

text:
Sport
Organization
Duration

Lacrosse
MLL
60 seconds

NLL
30 seconds

Ringette
N/A
30 seconds

Water polo
FINA
30 seconds

Canoe polo
ICF
60 seconds

Ten-pin bowling
PBA
25 seconds

Snooker
Snooker Shoot-Out
15 seconds (first five minutes)
10 seconds (last five minutes)

Carom billiards
(Three-cushion billiards)
World Championship
European Championship
World Cup
40 seconds[24]
(3 time-outs (40 sec.) possible)

text: Similar rules in basketball[edit]

text: The shot clock and its enforcement is used in concert with the rule that requires an offensive team to advance the ball across half-court and into the offensive zone (or front court) within a referee's count (this rule was first introduced in 1933, predating the shot clock by over 2 decades). In men's college basketball, the offense must advance the ball to the front court within 10 seconds, the same length used by FIBA and the NBA until they adopted an 8-second limit in 2000 and 2001, respectively. Failure by the offense to advance the ball to the front court within the time limit results in a turnover to the other team.

text: Generally, the 10-second (or 8-second) count is independent from the shot clock's operation; in fact, a referee may count the 8 or 10 seconds through a visible motion of his hand or arm. Women's college basketball introduced the 10-second limit in 2013–2014, and provided that officials will not count the ten seconds but "will use the shot clock to determine if a 10-second violation has occurred." As a general reference, it refers to the shot clock reaching 15 (FIBA/[W]NBA; because the NBA shot clock registers tenths in the final five seconds, the violation occurs once the clock registers 15.9 seconds on the console, which is posted as 15 on the clock) or 20 (college) before a violation can be called.[25]


document_title: Bill of Rights 1689

question_text: when was the english bill of rights created

text: Bill of Rights 1689

text: Background[edit]

text: During the early modern period, the power of the Parliament of England continually increased. Passage of the Petition of Right in 1628 and Habeas Corpus Act in 1679 established certain liberties for subjects. The idea of a political party took form with groups debating rights to political representation during the Putney Debates of 1647. The English Civil War (1642–1651) was fought between the King and an oligarchic but elected Parliament.[3][4][5]

text: Glorious Revolution[edit]

text: In the Glorious Revolution of 1688, a group of English Parliamentarians invited the Dutch stadtholder William III of Orange-Nassau (William of Orange) to overthrow King James II of England (James VII of Scotland and James II of Ireland). William's successful invasion with a Dutch fleet and army led to James fleeing to France. In December 1688, William took over the provisional government by appointment of the peers of the realm, as was the legal right of the latter in circumstances when the King was incapacitated, and summoned an assembly of certain members of parliament. This assembly called for an English Convention Parliament to be elected, which convened on 22 January 1689.[6][7]

text: Declaration of Right[edit]

text: The proposal to draw up a statement of rights and liberties and James's violation of them was first made on 29 January 1689 in the House of Commons, with members arguing that the House "cannot answer it to the nation or Prince of Orange till we declare what are the rights invaded" and that William "cannot take it ill if we make conditions to secure ourselves for the future" in order to "do justice to those who sent us hither". On 2 February a committee specially convened reported to the Commons 23 Heads of Grievances, which the Commons approved and added some of their own. However, on 4 February the Commons decided to instruct the committee to differentiate between "such of the general heads, as are introductory of new laws, from those that are declaratory of ancient rights". On 7 February the Commons approved this revised Declaration of Right, and on 8 February instructed the committee to put into a single text the Declaration (with the heads which were "introductory of new laws" removed), the resolution of 28 January and the Lords' proposal for a revised oath of allegiance. It passed the Commons without division.[8]

text: On 13 February the clerk of the House of Lords read the Declaration of Right, and the Marquess of Halifax, in the name of all the estates of the realm, asked William and Mary to accept the throne. William replied for his wife and himself: "We thankfully accept what you have offered us". They then went in procession to the great gate at Whitehall. The Garter King at Arms proclaimed them King and Queen of England, France and Ireland, whereupon they adjourned to the Chapel Royal, with the Bishop of London preaching the sermon.[9] They were crowned on 11 April, swearing an oath to uphold the laws made by Parliament. The Coronation Oath Act 1688 had provided a new coronation oath, whereby the monarchs were to "solemnly promise and swear to govern the people of this kingdom of England, and the dominions thereunto belonging, according to the statutes in parliament agreed on, and the laws and customs of the same". They were also to maintain the laws of God, the true profession of the Gospel, and the Protestant Reformed faith established by law.[10] This replaced an oath which had deferred more to the monarch. The previous oath required the monarch to rule based on "the laws and customs... granted by the Kings of England".[11]

text: Provisions of the Act[edit]

text: The Declaration of Right was enacted in an Act of Parliament, the Bill of Rights 1689, in December 1689.[12] The Act asserted "certain ancient rights and liberties" by declaring that:[13]

text:
the pretended power of suspending the laws and dispensing with laws by regal authority without consent of Parliament is illegal;
the commission for ecclesiastical causes is illegal;
levying taxes without grant of Parliament is illegal;
it is the right of the subjects to petition the king, and prosecutions for such petitioning are illegal;
keeping a standing army in time of peace, unless it be with consent of Parliament, is against law;[nb 2]
Protestants may have arms for their defence suitable to their conditions and as allowed by law;
election of members of Parliament ought to be free;
the freedom of speech and debates or proceedings in Parliament ought not to be impeached or questioned in any court or place out of Parliament;
excessive bail ought not to be required, nor excessive fines imposed, nor cruel and unusual punishments inflicted;
jurors in trials for high treason ought to be freeholders;
promises of fines and forfeitures before conviction are illegal and void;
for redress of all grievances, and for the amending, strengthening and preserving of the laws, Parliaments ought to be held frequently.

text: The Act declared James' flight from England following the Glorious Revolution to be an abdication of the throne. It listed twelve of James's policies by which James designed to "endeavour to subvert and extirpate the protestant religion, and the laws and liberties of this kingdom".[14] These were:[15]

text:
by assuming and exercising a power of dispensing with and suspending of laws and the execution of laws without consent of Parliament;
by prosecuting the Seven Bishops; by establishing of the court of commissioners for ecclesiastical causes;
by levying taxes for the use of the Crown by pretence of prerogative as if the same was granted by Parliament;
by raising and keeping a standing army within this kingdom in time of peace without consent of Parliament;
by causing Protestants to be disarmed at the same time when papists were both armed and employed contrary to law;
by violating the freedom of election of members to serve in Parliament;
by prosecutions in the Court of King's Bench for matters and causes cognizable only in Parliament, and by divers other arbitrary and illegal courses;
by employing unqualified persons on juries in trials, and jurors in trials for high treason which were not freeholders;
by imposing excessive bail on persons committed in criminal cases against the laws made for the liberty of the subjects;
by imposing excessive fines and illegal and cruel punishments;
by making several grants and promises made of fines and forfeitures before any conviction or judgment against the persons upon whom the same were to be levied;
all which are utterly and directly contrary to the known laws and statutes and freedom of this realm.

text: In a prelude to the Act of Settlement to come twelve years later, the Bill of Rights barred Roman Catholics from the throne of England as "it hath been found by experience that it is inconsistent with the safety and welfare of this Protestant kingdom to be governed by a papist prince"; thus William III and Mary II were named as the successors of James II and that the throne would pass from them first to Mary's heirs, then to her sister, Princess Anne of Denmark and her heirs (and, thereafter, to any heirs of William by a later marriage).

text: Date and title[edit]

text: The Bill of Rights is commonly dated in legal contexts to 1688. This convention arises from the legal fiction (prior to the passage of the Acts of Parliament (Commencement) Act 1793) that an Act of Parliament came into force on the first day of the session in which it was passed. The Bill was therefore deemed to be effective from 13 February 1689 (New Style), or, under the Old Style calendar in use at the time, 13 February 1688. Under the Short Titles Act 1896, the Bill was given the official short title of "The Bill of Rights", without a calendar year suffix.[16]

text: Augmentation and effect[edit]

text: The Bill of Rights was later supplemented by the Act of Settlement 1701 (which was agreed to by the Parliament of Scotland as part of the Treaty of Union). The Act of Settlement altered the line of succession to the throne laid out in the Bill of Rights.[17] However, both the Bill of Rights and the Claim of Right contributed a great deal to the establishment of the concept of parliamentary sovereignty and the curtailment of the powers of the monarch.[18][19][20] Leading, ultimately, to the establishment of constitutional monarchy,[21] while also (along with the penal laws) settling the political and religious turmoil that had convulsed Scotland, England and Ireland in the 17th century.

text: The Bill of Rights (1689) reinforced the Petition of Right (1628) and the Habaes Corpus Act (1679) by codifying certain rights and liberties. The rights expressed in these Acts became associated with the idea of the rights of Englishmen,[22] and described as Fundamental Laws of England. The Bill of Rights directly influenced the 1776 Virginia Declaration of Rights,[nb 3] which in turn influenced the Declaration of Independence.[23]

text: Although not a comprehensive statement of civil and political liberties, the Bill of Rights stands as one of the landmark documents in the development of civil liberties in the United Kingdom and a model for later, more general, statements of rights;[11] these include the United States Bill of Rights, the French Declaration of the Rights of Man and of the Citizen, the United Nations Universal Declaration of Human Rights and the European Convention on Human Rights.[24][25] For example, as with the Bill of Rights 1689, the US Constitution prohibits excessive bail and "cruel and unusual punishment". Similarly, "cruel, inhuman or degrading treatment or punishment" is banned under Article 5 of the Universal Declaration of Human Rights and Article 3 of the European Convention on Human Rights.

text: Legal status[edit]

text: The Bill of Rights remains in statute and continues to be cited in legal proceedings in the United Kingdom and other Commonwealth realms, particularly Article 9 on parliamentary freedom of speech.[26][27] Following the Perth Agreement in 2011, legislation amending the Bill of Rights and the Act of Settlement 1701 came into effect across the Commonwealth realms on 26 March 2015 which changed the laws of succession to the British throne.[nb 4]

text: Part of the Bill of Rights remains in statute in the Republic of Ireland.

text: United Kingdom[edit]

text: The Bill of Rights applies in England and Wales; it was enacted in the Kingdom of England which at the time included Wales. Scotland has its own legislation, the Claim of Right Act 1689, passed before the Act of Union between England and Scotland. There are doubts as to whether, or to what extent, the Bill of Rights applies in Northern Ireland.[26][nb 5]

text: On 21 July 1995 a libel case brought by Neil Hamilton (then a member of parliament) against The Guardian was stopped after Justice May ruled that the Bill of Rights' prohibition on the courts' ability to question parliamentary proceedings would prevent The Guardian from obtaining a fair hearing. Section 13 of the Defamation Act 1996, was subsequently enacted to permit MPs to waive their parliamentary privilege and thus cite their own speeches if relevant to litigation.[30]

text: Following the United Kingdom European Union membership referendum in 2016, the Bill of Rights was quoted in a court ruling on a legal challenge seeking a judicial declaration that triggering EU exit must first be authorised by an act of Parliament.[31][32]

text: Australia[edit]

text: The ninth article, regarding parliamentary freedom of speech, is actively used in Australia.[26]

text: Canada[edit]

text: The article on parliamentary freedom of speech is in active use in Canada.[26]

text: New Zealand[edit]

text: The Bill of Rights was invoked in New Zealand in the 1976 case of Fitzgerald v Muldoon and Others,[33] which centred on the purporting of newly appointed Prime Minister Robert Muldoon that he would advise the Governor-General to abolish a superannuation scheme established by the New Zealand Superannuation Act, 1974, without new legislation. Muldoon felt that the dissolution would be immediate and he would later introduce a bill in parliament to retroactively make the abolition legal. This claim was challenged in court and the Chief Justice declared that Muldoon's actions were illegal as they had violated Article 1 of the Bill of Rights, which provides "that the pretended power of dispensing with laws or the execution of laws by regal authority...is illegal."[34]

text: Republic of Ireland[edit]

text: The Act was retained in the Republic of Ireland although sections were repealed by the Statute Law Revision Act 2007 section 2(2)(a),[35] and Part 2 of Schedule 1.[36] Section 2(3) of that Act repealed:

text:
all of the Preamble down to "Upon which Letters Elections having been accordingly made"
the seventh paragraph "Subjects’ Arms. That the Subjects which are Protestants may have Arms for their Defence suitable to their Conditions and as allowed by Law."
all words from "And they doe Claime Demand and Insist" down to, but not including, section 2, bars Roman Catholics from Crown or Government, succession et cetera.

text: Modern recognition[edit]

text: Two special designs of commemorative two pound coins were issued in the United Kingdom in 1989 to celebrate the tercentenary of the Glorious Revolution. One referred to the Bill of Rights and the other to the Claim of Right. Both depict the Royal Cypher of William and Mary and the mace of the House of Commons, one also shows a representation of the St Edward's Crown and the other the Crown of Scotland.[37]

text: In May 2011, the Bill of Rights was inscribed in UNESCO's UK Memory of the World Register.[24][38]

text: As part of the Parliament in the Making programme, the Bill of Rights was on display at the Houses of Parliament in February 2015.[39]