logging in or signing up dna repair mechanism mrlonely Download Post to : URL : Related Presentations : Let's Connect Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Copy embed code: Embed: Flash iPad Dynamic Copy Does not support media & animations Automatically changes to Flash or non-Flash embed WordPress Embed Customize Embed URL: Copy Thumbnail: Copy The presentation is successfully added In Your Favorites. Views: 4597 Category: Education License: All Rights Reserved Like it (3) Dislike it (0) Added: June 23, 2010 This Presentation is Public Favorites: 1 Presentation Description No description available. Comments Posting comment... Premium member Presentation Transcript DNA REPAIR MECHANISM : DNA REPAIR MECHANISM Presented by Birendra kumar H. MS Ramaiah College, Banglore Flow of the Seminar : Flow of the Seminar Damage Repair mechanism Basic mechanism Of Repairing DNA Proteins involved Base Excision Repair Nucleotide excision repair Damage reversal Mismatch Repairing Double stand break SOS diseases How DNA are Damage : How DNA are Damage Mismatched bases Polymerase error rate about 1 in 104 Deamination of C to U leading to mismatch Missing bases. Hydrolysis of purine-deoxyribose bond leading to AP-site. Structural damage. Dimer formation. Broken phosphodiester bonds. Chemicals or radiation REPAIR MECHANISMS NECESSARY FOR SURVIVAL Types of DNA Damage Summarised : Types of DNA Damage Summarised Types of Repair Mechanisms : Types of Repair Mechanisms Damage Reversal- removal of dimers Double Strand Break- Recombination Excision Repair- Base Excision Nucleotide Exicision SOS Repair Mechanisms- Last line of Defense Proteins Involve in Repair Mechanisms : Proteins Involve in Repair Mechanisms Slide 7: The MutS protein of Escherichia coli MutS is responsible for recognizing and binding to base pair mismatches, and recruits other key proteins (MutH and MutL) required for repair to the mismatch site. ATP Proteins involve in Base Excision : Proteins involve in Base Excision UvrA and UvrB scan DNA to identify a distortion UvrA leaves the complex,and UvrB melts DNA locally round the distortion UvrC forms a complex with UvrB and creates nicks to the 5’ side of the lesion DNA helicase UvrD releases the single stranded fragment from the duplex, and DNA Pol I and ligase repair and seal the gap Slide 9: Excision repair........ OR Nucleotide excision repair : Nucleotide excision repair Two excinucleases (excision endonucleases) bind DNA at the site of bulky lesion. One cleaves the 5’ side and the other cleaves the 3’ side of the lesion, and the DNA segment is removed by a helicase. DNA polymerase fills in the gap and DNA ligase seals the nick. Damage Reversal : Damage Reversal Photoreactivation (the enzyme DNA potolyase captures energy from light ) Mismatch Repair : Mismatch Repair Mismatch repair deals with correcting mismatches of the normal bases; that is, failures to maintain normal base pairing (A･T, C･G) Recognition of a mismatch requires several different proteins including one encoded by MSH2. Cutting the mismatch out also requires several proteins, including one encoded by MLH1. Double Strand Break Mechanisms : Double Strand Break Mechanisms Damage in the DNA template can lead to DSB formation during replication The SOS Hypothesis : The SOS Hypothesis Radman 1974 originally proposed an inducible repair system Requires RecA and a regulator system Repair normally at low level lexA gene identified as a regulator Recombine normally But NO increased UV mutagenesis (ie 30 dimers produces no extra mutants). Higher doses required LOW DOSE - Error-free repair HIGH DOSE - Error repair INDUCED LexA is an autoregulated repressor Represses level of activity of many genes Collectively called DNA Inducible (din) genes Includes uvrA,B,C,D and sfi etc... RecA protease activity; Cleaves LexA Also CI repressor inducing lysis Slide 15: SOS System in E.coli Low level expression HIGH level expression Diseases : Diseases cellular ultraviolet sensitivity Werner syndrome (premature aging, retarded growth) Bloom syndrome (sunlight hypersensitivity) colon cancer Slide 17: Xeroderma pigmentosum Autosomal recessive mutations in several complementation groups Extreme sensitivity to sunlight Predisposition to skin cancer (mean age of skin cancer = 8 yrs vs. 60 for normal population) You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.