第二十二章DNA的复制-(精品课件).pptVIP

* 20 * 20 * SOS Repair-Error-prone replication The SOS repair system is induced in response to major damage to the bacterial DNA or in response to agents which inhibit DNA replication. The system is a complex one with over 20 genes involved. Two of these are the important regulator genes: lexA and recA. LexA is a repressor（阻遏蛋白） that regulates the expression of all of the other SOS repair genes, including recA. It also regulates its own synthesis. LexA is a dimer. Each monomer has a DNA binding domain and a dimerization domain, however, the protein will not bind to DNA unless it has formed a dimer first. Normally, LexA binds to its operators（操作子） to block expression of the SOS repair genes. The RecA protein is a multifunctional protein with ATPase and ssDNA binding activities. When bound by ssDNA, it is also a co-protease. Damage or severe stress to the cell generates ssDNA which activates this co-protease（共蛋白酶） activity. The RecA co-protease activity stimulates the protease activity of the LexA protein. The autocleavage of LexA separates the DNA binding domain from the dimerization domain. As a result, LexA is no longer able to repress transcription; the SOS repair genes are thereby induced and expressed. Among the genes that are induced are umuC and umuD. UmuD is cleaved by the RecA coprotease activity and the truncated protein, UmuD, in association with UmuC forms DNA polymerase V (D2C) which replicates past gaps in the DNA without the proofreading functions of PolIII. UmuD2C is a relatively poor polymerase that synthesise DNA distributively. PolV requires the β andγ subunit of PolIII for optimal activity. β, which functions as the sliding clamp, is required for processivity and γ is the clamp loader. DNA synthesis by PolV is error-prone. Is there any similar SOS response in human bodies? DNA damages P53 P21 The cell cycle is arrested and stays at G1 Repair before DNAs replicate Too severe to repair Apoptosis will be induced Damaging agents Recombinational