Lecture 10 Notes
Lecture 10 Notes BIOL-L211 2521
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This 12 page Class Notes was uploaded by AnnaClippinger on Friday October 16, 2015. The Class Notes belongs to BIOL-L211 2521 at Indiana University taught by Megan Dunn in Summer 2015. Since its upload, it has received 27 views. For similar materials see Molecular Biology in Biology at Indiana University.
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Date Created: 10/16/15
Til ES Cl all 1 El 5 Dtom rm Nuclth eel ll Nj ill b u N tickle Rel ll Lecture 10 39 Last Time llello mothers hello father Replication Initiation Replication and the Mismatch Repair System 39 Today a Corrupt DNA might be good for you MDIECUIGT BIOIUQVI lh thtL39NENE Chemical and Environmental lVIutagens Bgudln m gl gnmmr Cellular Damage Mechanisms Ch m pqq 71M 3 Double Stranded Breaks 39 Next Time Reading Assignment 1 rill j r gt r r I Transcription in Prokaryotes EXom Wrapper i Goals Identify the informational sourcels of missed questions Identify the strategies to make information more meaningful and memorable Generate study plan based on error patterns Approximately how much time did you spend preparing forthi s exan39l What percentage of yourtestpreparation was spent in each ofthese activities Readlng textbook sectionls for the first time 7 ti H 0w mum fl me i r llDUl REA LN swarm t tudxl 2 u a Rereading textbook sections Reviewing time to think exercises Reviewing probllem set answers Ans wering weekly review questions Reviewing key terms I Reviewingvour own notes Reviewing molecular biology in the new articles Other specify Exam Wrapper quot l Now that you have looked over yOu39r graded exam estimate the percentage of points youlost due to each of the folllowing39 Careless mistakes marked the wrorlg answer Misread the question Did not know all vocabulary to correcth choose an answer Lack of understanding of the concept Other specify 7 1 Need to provide M are damn Estimate the peroEntage of point you lost due to the folloWing Lecture 1 39 Lecture 2 Lecture 3 0F Lem 4 Exam Wl ll to aw in ith Game Lecture 5 for m Lecture 6 Lecture 7 Lecture 8 Molecular biology in the news Whale 1E m Me 9mm l39 Corrupt DNA Might Be Good For Youquot 1 5cien cAmericon Quanta Magazine Sept 2014 N T from an Identical qmu mm a a a as wwheh w M quot Genetic diversity exists 7 a r r g comparing Wl 0 fquot Qrwlug qch f Might make us more adaptive and resilient a a V 7 WI Brain cell from embryonic mouse 3 copies of chromosome 2 one copy of 15 and 17 we Gus Igctkdded f W m N mall O39N39l39 OF Human 39 7 b H ormm r r I n re e f I 1 a 3 quot fquot V 7vquot 1quot m V 39 39 r quot 39 T1 r a iiir aerial Irvlf39 injury r 7 u1 39 u L TV 3 Wm 31 T 23 f1 V ellh u i way 5 gt I a r 39139 Vquot H H m quot e r it an t Fl Th llLu39ui ll nl tlllalquot lill39 lm39rjl r39quotm l 1 quot 39 39m 9 vs I39d39 i5 3 L gt11 a armd c v r 1 r u n r l r l 39 r l l 1M L L 7 l Assists In disease recovery Though scientists disagree over extent of variabilityan bene ts 4 k H mm 101 is H rel 401quot x we study 11 Mums Mat onon by mutogens Replication errors can cause mutations but so can mutagens DNMuh m dawqu busomemms f 39 in tnttntlmnmurl That the UM l9 Ex P efdl39m Nl 39lugr mumrm Mr damage W 39 man Brittlel or Enwrunmma moans Ultra Gamma and X rays Chemical mutagens Reactive oxygen species produced from normal metabolic processes quot39739 1iquot I 7 quot v 41 u x i 39lLquot 39139a i39Z39 m silt 5795 Jere Chemical modifications of bases Formation of nucleotide dimers Formation of doublestranded breaks Strategies by the cell The cell has numerous s 7and backup plans to repair damage caused by chemical and environmental mut agehst MON tht Quutl isomer We will discuss Base excision repair system u Fail sate glycosvlases Nucleotide excision repair system N ER Transcription coupled repair Error prone polymerasestranslesion synthesis DNA photolvase Methvltransferase a Nonahomologous end joining Homologous recombination Sta rt learning these systems anal the protein namesfunctions your life much easier later 1 r m m wquot Chemical modification fb awe f f x so ases m E W 39 f co m Victim fact w Hmr wearJ Bases can be chemically modi ed blTutagens 7 Md39tnlnonrrtctaa Pdvfnae e w e r 39 Ha2meah WW a w i r a Wm W 1 WW m mmtl lldku azcmmrml 1 quotFWW n reqc oh nwh C W 39 mtnn 6f39 A zjmmonmj I39m i agbg m memo d Iquot MdchPnFMuim agar guinifnr IncrmfmfjmH I a Jy Em R lidam Fiag r39e39h f w d WW g um 39 quotTa H Au 1 a Prolqumumc he quot Tm 0 N wmmw 13W wgaaw mm mm Examples i strand mm def 9 7 H commLoa nan n Wi ll l ll 7 BgxaGA base pair fa WrrJ v g U 33565quot EaI1 also be 3 31 v a T ZT Hlom 1amp9 nquot A lIlf Dingo LIT fang w E39gt nc m mp e w 1 ll rlnquot m m l Nquot wncorpummnofn on 099on SM W few g p I H qrruM quot A Tram fan Base excisianv rapair repiacing damaged nutleo des we on Heirmt Fsdm WW9 Damag39edg cam be removed and replaced lays Recognizes a specific damage base cleaves mwwqidrc 50nd a v V 39 539 I geeee Eva nee 7 39 sle r i 7 39 here fr 039 2f0rms 39 39 7 hot11 GUgan ang Abmcq I 1 has 1an a 1 WWW e W razwcgrmsmmmu cult 39 u I Single strand of DNA shownH 900911 Base excision repair repiacing damaged nucleotides cont Da maged muw Riigw bumm at L g iquot j i 0 fhvp leaving me 7 AP ando oieaves here M 39 iimakesauoHrcr NI gt replaces the base Ami 0 9 1 M 31123 WIMP i nave ma gm mm m in here lager ma keg the phasphodiester Fig 1043 a Singie strand of DNA sihiownl i i Base excision repair replacing damaged nucieofides f I 39 Swnnmg m ans Tm M In a C1 Wilkfk How do i cog iases recognize damagedbases 4 r I inquot w t ne mmbrqLh uahfnr 9m 1 DNH un m deem GP q m WWQWHWH W m m0an How do giycosyioses remove damaged bases The clamqued bust rammed will Hum ml an mm x 395 New m m QN C091 lag Unirti are Glycasvlase Damaged base i i DNA Fig 10 714 10 Role offailasafe DNA glycosyiases N 9mm Thru inc Mmm 1mm scan DNA for bases that were overlooked by base39ei ci Sion repair NW N Criniheamd BM Example Guanine base that has undergone oxidation BM in win Fail safe glycosylase recognizes GA pair a a V quot quot i M i 0 5 v 7 2 IC 39 39 i A v i quot4 V i v 3939 3 e 393 for 2 E V 390 g 39 a V i A quot391 l quot p i Cr i H i 1 I i i 1 i 2 i quot5quot V E 39 r i 3 Lquot KE in C In i if plan no A Rep mm M BERQTI Ill NEEaEDH 39 rig 1045 Nucieo de excision repair removal of thymine dimers 7 I kg looking for a GpEiii ic lea ion iwgii kim in ii BM n 39 Fusion oftwo tin inesroaused i3 UV radiation i quot E37 V 39 I 7 y i H Li bmggiymerase malepgflring reiniiacio P WI c ii nnni quot Bach pai r WWW QM m T i u v N H RH thymine dimer Em 109 Recognized a mi removed by unlike BER nuoieotide excision repair does not recognize anvst eo a lesion m V Recnq N Lee en qruri wire in r nmmps oi Fm nuns Hum 12 Nucleotide excision repair in coli dielerlien mdi turtilm Wm tGLP T W f LQI 17 e W t w WW r at M m w dl gto HI on MELTG TM 1qu WM defarh w 39leaves the comp ex x I 1l I r A h k39 L V quot 6 l I 1 III we y 1 I I 17 creates a bubble around the distortion f makes singlestranded nicks on mquot sides ofwthe distortion r r H r i x t D m T mm an End 0 nudee Juc r om MI I met J 3V7J hellicase removes the single strand fragment N0 we m w an opening DNA 7 I39meliceee Jer DNAperrnerase 39 D39MA HQESE v 39 Fig 10 16 14 Transcriptioncoupled repair What happens rfNER misses a distorted base I RN Pl WNWth Will Titania rm diam t in during transcription 39 it26quotEtna339113quotquotquot51 I f A N Mead Ji slrli lf aalFx l f iti at l Ir v tr nucleotide excision i a gt quot lt to pair proteins INN or Error prone polymerases BER and NER are not 100 ef cient if DNA polymerase erleotlnters thy minefggimers ring replication replication DNA polymerase Ill m RNA Problem 3395quot 1 NA polymerase stalls a1 distortion i ltlls Numho E meioh RtpdlrlN39ER in wrmm Marl I c lsl lsam tat 4 Puri ed hat we rd to mm a DNA is not fully replioatedF replication machinery cannot bypass the distortion Solution There are advantages and disadvantages w Moanml Wrong E Gt N p pow mtm cg in r u 1i lit v 16 l i Rt rum NE R P mama to rm Ci ll 3 all RN Wl l mll i t MET MW LMfi m rm Ell l l il Calm dig Mon Em R PW lun V AIyll J 5 31F 51 Mtrev MW I it II i IL I 39 39 quot quot quot739 Tmnslesion synthesis DNA polymerase III E to Re jv licatiesn sta lie at thyrn 0U my 1 35 dimers in in Mint airmen 1 Beclamp m Pei l Pol IV Din E UmuD39ZC 9 Which Replaced by quot mph mite B VER me rmmrm r MM plum N Mm mini Mu Irmm i pm 99911 w 7 Error rene Mel rnerase ldisseciates Replaced by original DNA polymerase Realm waahr mgent 39Liuib if ilthl Rep an path male medal 1 DNA polymerase dissociates Ber 7 5i Al frrnah tC Mil J5 Removing thymine dimers with DNA photolyase NER proteins recognize and repair thymine dimer distortions mirth w l l Tilt com mrranr39q But thymne dimers form at quotvery high frequency Additional mechanisms needed Q rqv 39r fm TO BE GC39l39l fC l lieBill m E KPO 9 Ed V l 9i ME liq ill a s reverses formation efthyrnine dimers WNW GIN German in the 2 rm mm Ree id leg UV Fig 10 11 18 Removing methylated nucleotides j I 39 Meth latienef guanine can adepta new structure ma impre erl base air CIHUWDI Had V V p V p a W lit d ch l39llHrlli w wquot M th Pans V V I I aquot 1 HI quot DNA polymerase reads quot 39 an Em 7 39 SEMI methylated asAr 39 gnu aha H H Ermine l ll N T m quot 7 Us distortion too small to berecegnizecl by NER I s rem II wt MemeI qro u P i 4 mm N h I III W in I lit Mad W Eggi l Ba 0r q meiiryllraflaferase I Fig 1042 1939 Double stranded breaks DSBS 77 s e f are one ofthe most toxic farms of DNAdamage B M Trim 93301 P39hoclphudIeIor Ema 39 If Nut RepalrEICEIQUES39lkhN I 7 7 V l 7 W ii JTilliligallfir I I I I I I II I I I II I I II I I I I I I IhIu mmmm Phxesphediester bends break can also result in deletions If net repaired the cell will die during DSBs result b I MIWGI QMK van was imms oi RadIuIIrIn memes Phil ilfall tomrrcllnls RUIN I Irr om qm 9 paces 2D D Eta 5 Double 9 tangled Bream Reactive oxygen species can cause D535 2 oxygen 4 I Produced by Metabotism M ammq ow gen at 19 commm dealth wl f 039 39 Ham mu WE ml q m mummies immune system ELL mm of Rad39iatiotl t 39 Mauumoltcmta Superoxide reacts with and damages aj macromotecules it comes into contact with t M091 c mm on tam I9 NH can c He mm lw Mueer mm a 39r mug DS 39 W ibteawch hydragen peroxide H202 21 053 rEpair mechaniSms I i mn lugmm 7 DNA Nontmmolaggus em joining quotI l Imimlmgmm recmtthinatitm ckup DSB system in some organisms JOIN Ramktnth M Ma tnqtmer Typicallly the principatl pathway used to repairDSB r a a H mm Inc we C hmm mamas prawn temp mnt nt Rapulr R949 W i H game mumth39um as 2th 3k N0 twp lat qu39idmg 4mm 90 H at ten can Nonh0m0logou5 endjoinfng NHEJ An overview 5 TGACGATGCTTGAC 3 3quot ACTGCTACGAACTG 5 l 39 quot 39 39 Double stranded break 4 THEN med wcrw u Reqmn 0f 3 53213523 ESE5123 quan tuned me Reqtctwn i 5 E DTGACGAT 3 3 F CGAACTG H 5 l u n7 39 391 1 2 I mm quotlong we 9H m wuu a log Wit 170 FM WEMCNIQELHUH 0f 39 5 TGAC 3 339 e ACTG 5 W39 6 1 to expose ssDNA kmuam L TMiLG m1 39 Eurum 0H mm M mm W5 339 ifquot TGAC3 Than JUGHWP of ma mm cm ACTGa 5quot Wu W egemtwtw New camwc 0F Nonhomologous end joining NHEJ New with proteins dqublerstrand break in DNA 1 Resec n exnoses small ions of ssDNA IEND nacoemnam BY II lac RM 09 n I2 1 WM m Ru HETEHDDIMERS m f form hehe o dimer RELIHH uddit I and DVD 11 m 1 ADDITIONAL PRUTEINS lenocessms 0F DNA ENDS Ends mug t thether 399 End processing LigatiDn w m hf talcum gnome DNM pmmm lLfMITED REPAIR SYNTHESIS l MGATIDM 39 39 Ir repaired DNA has generally suffered a deletion of nucleotides 24f INCI