Structural Biology of DNA Damage and Repair

126 Pages·2010·3.877 MB·English

by  Michael P. Stone (Eds.)

Structural Biology of DNA
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In Structural Biology of DNA Damage and Repair; Stone, M.;
ACS Symposium Series; American Chemical Society: Washington, DC, 2010.
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In Structural Biology of DNA Damage and Repair; Stone, M.;
ACS Symposium Series; American Chemical Society: Washington, DC, 2010.
1041
ACS SYMPOSIUM SERIES
Structural Biology of DNA
Damage and Repair
Michael P. Stone, Editor
Vanderbilt University
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Sponsored by the
ACS Division of Chemical Toxicology
AmericanChemicalSociety,Washington,DC
In Structural Biology of DNA Damage and Repair; Stone, M.;
ACS Symposium Series; American Chemical Society: Washington, DC, 2010.
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bs.acs.or0-1041.f Strucpt.ucrmal.b-i-ol(oAgCySofsyDmNpAosdiaummasgeeriaensd;r1e0p4a1ir)/MichaelP.Stone,editor.
pu01 Includesbibliographicalreferencesandindex.
p://k-2 ISBN978-0-8412-2574-9(alk.paper)
2 | htt021/b 1Q.HD4N6A7.Sre7p7a2ir0-1-C0ongresses.2. DNAdamage--Congresses. I.Stone,MichaelP.
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PRINTEDINTHEUNITEDSTATESOFAMERICA
In Structural Biology of DNA Damage and Repair; Stone, M.;
ACS Symposium Series; American Chemical Society: Washington, DC, 2010.
Foreword
The ACS Symposium Series was first published in 1974 to provide a
mechanism for publishing symposia quickly in book form. The purpose of
the series is to publish timely, comprehensive books developed from the ACS
sponsoredsymposiabasedoncurrentscientificresearch. Occasionally,booksare
developed from symposia sponsored by other organizations when the topic is of
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In Structural Biology of DNA Damage and Repair; Stone, M.;
ACS Symposium Series; American Chemical Society: Washington, DC, 2010.
Preface
Thehumangenomeiscontinuouslyexposedtomanyclassesofgenotoxins.
Of these, three that will be discussed herein include 5,6-dihydroxy-5,6-
dihydrothymine (thymine glycol; Tg), O6-methylguanine (O6MeG), and
benzo[a]pyrene. Thymine is highly susceptible to oxidative damage and Tg,
formsbyreactionofthyminewithreactiveoxygenspecies. Tghasbeendetected
1
ubs.acs.org 10-1041.pr00 iotanhdfedtauhTncyigtmmslaiepnlsleiaaoyngnsdly(uc3hpo)uolminllleausnmsitoorunadrstiuenlpeate;thirneigtdraoibyslieoe(1lsoot,figm2icc)oa.atnlefidSrgetuutchrdoaaigtetinsohintouiaonmlnatihnnaetnecdrsectlrorluesncsvptrueeorrpnsaaisloierbn.ihoouPlfonugDdryriNendoeAssf
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2 | htt021/b dparomdaugcet binytthraengsfeenrorimnget(h4e).alkTyhlegOro6u-palktoylatrreaancstfievreasaecstifvuenscittieoncytsoterienveerresseidthuee
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une 0 | d (B[a]PDE) (6). In all cases, if the genome is not repaired, these and other
on J201 genotoxic lesions precipitate serious biological consequences, including altered
d by 89.163.35.42 ate (Web): June 1, gipctyerontiosfiesTliieennhxsceeprtrmedheaeasesvsttihineoaylgnorllea,pytmmiiobmuenentipant(rt7giioon).fntree,sdcaiotnebgd-ynscpiezenlecladitdfiuetcrhaaatlahltpy.pDIrnoNocaaAccduhdrleiretisisnoigtononwtDsoaNctrhdaAenmgmaeolntoneodirttioofitrxhciineacgtireoepcnshipsge,oemnnesie.cetgais.cl,,
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adn lesions situated at a known position within DNA, e.g., with respect to their
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wnlcati structures, and their replication (8, 9), have led to tremendous advances in
Dobli understandingofthechemicalbiologyofDNAdamage(10). Similarapproaches
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how thermal destabilization of the damaged DNA facilitates lesion recognition.
The structure of E. coli AlkA, which excises alkylated bases from DNA (4),
complexed with DNA containing pyrrolidine, reveals a protein-induced DNA
bendingconcomitantwithflippingofthealkylatedbase(11,12). Whenboundto
DNA containing 1-azaribose or ethenoadenine its human homologue AAG also
discriminatesbetweendamagedandnormalbasesviabaseflipping(13,14). Base
excision repair studies using DNA containing 8-oxoguanine complexed with
FAPy glycosylases suggest how these oxidative damage lesions are recognized,
and suggest the base-flipping mechanism by which excision occurs (15–22).
Human uracil-DNA glycosylases also flip the damaged base out into the active
site (23, 24). Likewise, the structure of endonuclease IV complexed with an
abasic site shows both the abasic site and its partner flipped out of the helix,
thuspromotingspecificinsertionandendonucleolyticcleavageoftheabasicsite
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In Structural Biology of DNA Damage and Repair; Stone, M.;
ACS Symposium Series; American Chemical Society: Washington, DC, 2010.
withintheactivesitepocket(25). Thus,thebaseflippingmechanismappearsto
becommontothebaseexcisionrepairprocess(26,27). Thefirststructuralviews
ofnucleotideexcisionrepairalsosuggesttheimportanceofbaseflippingintothe
activesitepocketoftherepairenzyme(28,29).
The impetus for this volume came from a recent symposium sponsored by
theACSDivisionofChemicalToxicology,bringingtogetherscientistsinterested
in the synthesis and structures of site-specific DNA adducts and in mechanistic
aspects of DNA repair. This volume presents work at the interface between the
structuralbiologyofDNAdamageandDNArepair.
In closing, I gratefully acknowledge support from the American Chemical
Society Division of Chemical Toxicology and the National Institute of
EnvironmentalHealthSciencesR13ES-016957.
1
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2 | http://p021/bk-20 2. A8U5d.S,e.2lAm7.0a16n9–,82R47.,0;88S1.a,u5l,6R33.–L5.6;3A7m. es,B.N.Proc. Natl. Acad. Sci. U.S.A.1988,
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une 0 | d 4. Lindahl, T.; Sedgwick, B.; Sekiguchi, M.; Nakabeppu, Y. Annu. Rev.
n J01 Biochem. 1988,57,133–157.
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by e ( Biochemistry2005,44,1054–1066.
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aden D 8. Basu,A.K.;Essigmann,J.M.Chem. Res. Toxicol. 1988,1,1–18.
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Pu 11. Hollis,T.;Ichikawa,Y.;Ellenberger,T.EMBOJ.2000,19,758–766.

12. Hollis,T.;Lau,A.;Ellenberger,T.Prog. NucleicAcidRes. Mol. Biol. 2001,
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Proc. Natl. Acad. Sci. U.S.A.2000,97,13573–13578.
15. Bruner,S.D.;Norman,D.P.;Verdine,G.L.Nature2000,403,859–866.
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18. Fromme,J.C.;Verdine,G.L.EMBOJ.2003,22,3461–3471.
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652–656.
20. Banerjee, A.; Yang, W.; Karplus, M.; Verdine, G. L. Nature 2005, 434,
612–618.
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In Structural Biology of DNA Damage and Repair; Stone, M.;
ACS Symposium Series; American Chemical Society: Washington, DC, 2010.
21. Banerjee,A.;Santos,W.L.;Verdine,G.L.Science2006,311,1153–1157.
22. Banerjee, A.; Verdine, G. L. Proc. Natl. Acad. Sci. U.S.A. 2006, 103,
15020–15025.
23. Parikh,S.S.;Mol,C.D.;Slupphaug,G.;Bharati,S.;Krokan,H.E.;Tainer,J.
A.EMBOJ.1998,17,5214–5226.
24. Slupphaug,G.;Mol,C.D.;Kavli,B.;Arvai,A.S.;Krokan,H.E.;Tainer,J.
A.Nature1996,384,87–92.
25. Hosfield,D.J.;Guan,Y.;Haas,B.J.;Cunningham,R.P.;Tainer,J.A.Cell
1999, 98, 397–408.
26. Mol,C.D.;Hosfield,D.J.;Tainer,J.A.Mutat. Res. 2000,460,211–229.
27. Yu,B.;Edstrom,W.C.;Benach,J.;Hamuro,Y.;Weber,P.C.;Gibney,B.R.;
Hunt,J.F.Nature2006,439,879–884.
28. Min,J.H.;Pavletich,N.P.Nature2007,449,570–575.
1 29. Scrima,A.;Konickova,R.;Czyzewski,B.K.;Kawasaki,Y.;Jeffrey,P.D.;
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xi
In Structural Biology of DNA Damage and Repair; Stone, M.;
ACS Symposium Series; American Chemical Society: Washington, DC, 2010.
Chapter 1
Overview
Michael P. Stone*
DepartmentofChemistry,VanderbiltUniversity,Nashville,TN37235
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bs.acs.or0-1041.c
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on June 21, 202010 | doi: 10. aaaaddrdidddsuuiuncccgtttsss.fraaorrEmiissxiinnacgmgelplffulrreoloasmmrinooaxxfltihidadiatsaottixivooievnnedroBvafim1e,wtahgayeolm,dfeianthnheyde.distchuIybnemjleeticucntrternio,ngpclhslyuuiclcdeohesl
d by 89.163.35.42 ate (Web): June 1, pecrexhrpoceacimsieriisocsonaifnlgDrterNopafanAisDrfdoNparrAmmocaadetgaiseomsnebassyg,emba.aansydemmexoacdyisuilmoantoedruethplaeatierreatchnoedgnnmiutuicotlaengoetainndidec
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Downloadblication Likethechameleon,DNAadductssometimeschangetheircolorationinthe
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formationofnewtypesofdamagehavingdifferentgenotoxicconsequencesthan
theoriginallyformedadducts.
Aflatoxin B (AFB ), a potent mycotoxin contaminating human foodstuffs,
1 1
is amongst the most mutagenic environmental chemicals to which humans
are exposed (1); it induces G→T mutations in Escherichia coli (2). The
N7-deoxyguanosine adduct formed in DNA by AFB epoxide (3, 4) undergoes
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chemical re-arrangement to the corresponding formamidopyrimidine (FAPY)
lesion. The significance of this chemistry with respect to the etiology of
humancancerassociatedwiththismycotoxinbecameapparentfromtwosetsof
observations. Earlyon,itwasrecognizedthattheFAPYformoftheAFB lesion
1
exhibited a significantly longer half-life in vivo (5). The longer half-life would
increase the potential for mutagenesis, but moreover, might suggest that the
lesionisrefractorytoDNArepair. Withrespecttorepair,AFB -FAPYlesionsare
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©2010AmericanChemicalSociety
In Structural Biology of DNA Damage and Repair; Stone, M.;
ACS Symposium Series; American Chemical Society: Washington, DC, 2010.