页数：58页文件大小：1.68 MB来源： 分子生物学基因Geneppt课件
本课件为《分子生物学》第14章重组与修复（Recombination and repair），依据 Gene VII 教材编排，沿Breakage等小节推进，讲解本章核心概念与分子机制，配逐页图示与文字版。
Chapter 14 Recombination and repair
Bivalent isthe structure containing all four chromatids (two representing each homologue) at the start of meiosis.
Figure 14.1 Recombination occurs during the first meiotic prophase. The stages of prophase are defined by the appearance of the chromosomes, each of which consists of two replicas (sister chromatids), although the duplicated state becomes visible only at the end. The molecular interactions of any individual crossing-over event involve two of the four duplex DNAs.
Figure 1.22 The ABO blood group locus codes for a galactosyltransferase whose specificity determines the blood group.
Figure 14.1 Recombination occurs during the first meiotic prophase. The stages of prophase are defined by the appearance of the chromosomes, each of which consists of two replicas (sister chromatids), although the duplicated state becomes visible only at the end. The molecular interactions of any individual crossing-over event involve two of the four duplex DNAs.
Figure 14.2 Recombination between two paired duplex DNAs could involve reciprocal single-strand exchange, branch migr at ion, and nicking.
Figure 14.3 Branch migr at ion can occur in either direction when an unpaired single strand displaces a paired strand.
Figure 14.4 Resolution of a Holliday junction can generate parental or recombinant duplexes, depending on which strands are nicked. Both types of product have a region of heteroduplex DNA.
Figure 14.5 Recombination is initiated by a double-strand break, followed by formation of single-stranded 3′ends, one of which migrates to a homologous duplex.
Figure 14.6 The synaptonemal complex brings chromosomes into juxt a position. This example of Neotelli a was kindly provided by M. Westergaard and D. Von Wettste in.
Figure 14.7 Double-strand breaks appear when axial elements form, and disappear during the extension of synaptonemal complexes. Joint molecules appear and persist until DNA recombinants are detected at the end of pachytene.
Figure 14.8 Spo11 is covalently joined to the 5′ends of double-strand breaks.
Figure 14.9 RecBCD nuclease approaches a chisequence from one side, degrading DNA as it proceeds; at the chi site, it makes an endonucleolytic cut, loses RecD, and retains only the helicase activity.
Figure 14.10 RecA promotes the assimilation of invading single strands into duplex DNA so long as one of the reacting strands has a free end.
Figure 14.2 Recombination between two paired duplex DNAs could involve reciprocal single-strand exchange, branch migr at ion, and nicking.
Figure 14.11 RecA-mediated strand exchange between partially duplex and entirely duplex DNA generates a joint molecule with the same structure as a recombination intermediate.
Figure 14.12 RuvAB is an asymmetric complex that promotes branch migr at ion of a Holliday junction.
Figure 14.13 Bacterial enzymes can catalyze all stages of recombination in the repair pathway following the production of suitable substrate DNA molecules.
Figure 14.14 Spore formation in the Ascomycetes allows determ in at ion of the genetic constitution of each of the DNA strands involved in meiosis.
Figure 14.14 Spore formation in the Ascomycetes allows determ in at ion of the genetic constitution of each of the DNA strands involved in meiosis.
Figure 14.15 Separation of the strands of a DNA double helix could be achieved by several means.
Figure 9.18 E. coli sigma factors recognize promoters with different consensus sequences. (Numbers in the name of a factor indicate its mass.).
Figure 14.16 Bacterial type I topoisomerases recognize partially unwound segments of DNA and pass one strand through a break made in the other.
Figure 14.17 Type II topoisomerases can pass a duplex DNA through a double-strand break in another duplex.
Figure 14.18 DNA gyrase may introduce negative supercoils in duplex DNA by inverting a positive supercoil.
attsites are the loci on a phage and the bacterial chromosome at which recombination integrates the phage into, or excises it from, the bacterial chromosome.
Figure 14.19 Circular phage DNA is converted to an integrated prophage by a reciprocal recombination between attP and attB; the prophage is excised by reciprocal recombination between attL and attR.
Figure 14.20 Does recombination between attP and attB proceed by sequential exchange or concerted cutting?.
Figure 14.21 Staggered cleavages in the common core sequence of attP and attB allow crosswise reunion to generate reciprocal recombinant junctions.
Figure 14.2 Recombination between two paired duplex DNAs could involve reciprocal single-strand exchange, branch migr at ion, and nicking.
Figure 14.22 Int and IHF bind to different sites in attP. The Int recognition sequences in the core region include the sites of cutting.
Figure 14.23 The Int binding sites in the core lie on one face of DNA. The large circles indicate positions at which methylation is influenced by Int binding; the large arrows indicate the sites of cutting. Photograph kindly provided by A. Landy.
Figure 14.24 Multiple copies of Int protein may organize attP into an int a some, which initiates site-specific recombination by recognizing attB on free DNA.
Figure 14.25 Substitutions of individual bases create mismatched pairs that may be corrected by replacing one base; if uncorrected they cause a mutation in one daughter duplex.
Figure 14.26 Modific at ions or removal of bases may cause structural defects that prevent replication or induce mutations in each replication cycle until they are removed.
Figure 14.14 Spore formation in the Ascomycetes allows determ in at ion of the genetic constitution of each of the DNA strands involved in meiosis.
Excision of phage or episome or other sequence describes its release from the host chromosome as an autonomous DNA molecule.
Figure 14.27 Excision-repair removes and replaces a stretch of DNA that includes the damaged base(s).14.12 Excision repair systems in E. coli.
Figure 14.28 The Uvr system operates in stages in which UvrAB recognizes damage, UvrBC nicks the DNA, and UvrD unwinds the marked region.14.12 Excision repair systems in E. coli.
Figure 14.28 The Uvr system operates in stages in which UvrAB recognizes damage, UvrBC nicks the DNA, and UvrD unwinds the marked region.14.12 Excision repair systems in E. coli.
说明：本页源文与上一页完全相同，疑为课件连续两页沿用同一页内容，已按原文保留。
Figure 14.37 A helicase unwinds DNA at a damaged site, endonucleases cut on either side of the lesion, and new DNA is synthesized to replace the excised stretch.14.12 Excision repair systems in E. coli.
Figure 14.29 A glycosylase removes a base from DNA by cleaving the bond to the deoxyribose.
Figure 14.30 A glycosylase hydrolyzes the bond between base and deoxyribose (using H20), but a lyase takes the reaction further by pening the sugar ring (using NH2).
Figure 14.31 A methylase "flips" the target cytosine out of the double helix in order to modify it. Photograph kindly provided by Rich Roberts.
Figure 14.32 Preferential removal of bases in pairs that have oxidized guanine is designed to minimize mutations.
Figure 13.30 Replication of methylated DNA gives hemimethylated DNA, which maintains its state at GATC sites until the Dam methylase restores the fully methylated condition.
Figure 14.33 GATC sequences are targets for the Dam methylase after replication. During the period before this methylation occurs, the nonmethylated strand is the target for repair of mismatched bases.
Figure 14.34 MutS recognizes a mismatch and translocates to a GATC site. MutH cleaves the unmethylated strand at the GATC. Endonucleases degrade the strand from the GATC to the mismatch site.
Figure 14.31 An E. coli retrieval system uses a normal strand of DNA replace the gap left in a newly synthesized strand opposite a site of unrepaired damage.14.16 Retrival systems in E. coli.
Figure 14.32 The LexA protein represses many genes, including repair functions, rec Aand lexA,. Activation of RecA leads to proteolytic cleavage of LexA and induces all of these genes.
Figure 14.32 The LexA protein represses many genes, including repair functions, rec Aand lexA,. Activation of RecA leads to proteolytic cleavage of LexA and induces all of these genes.
说明：本页源文与上一页完全相同，疑为课件连续两页沿用同一页内容，已按原文保留。
Figure 14.37 A helicase unwinds DNA at a damaged site, endonucleases cut on either side of the lesion, and new DNA is synthesized to replace the excised stretch.
Summary
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