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1、1 Repair of thymine dimers is that the daughter strands have large gaps. one for each unexcised thymine dimer. There is on way to produce viable daughter cell by continued replication alone because the strands having the thymine dimer will continued to turn out gapped daughter strands, and the first
2、 set of gapped daughter strands will be fragmented when the enters a gap. By a recombination mechanism involving sister-strand exchange, however, an intact double-stranded molecule can be made The essential idea sister-strand exchange is that single-stranded segment free of any defects is excised fr
3、om the homologous DNA segment and inserted into the gap produced opposite the thymine dimer (Figure 9-12).This genetic recombination event requires the RecA protein. DNA Pol I then synthesjzes the complementary strand, and DNA ligase joins this inserted piece to adjacent DNA, thus filling in the gap
4、. The gap formed by excision of one strand from the donor is repaired by DNA Pol I and DNA ligase. If each thymine dimer is repaired this way, two complete daughter single strands can be formed, and each can serve in the next round of replication as a template for synposite strands are near one anot
5、her because then no undamaged sister-strand segments are available to recombine with the other strand. Many molecular details of recombinational repair are still not known, so the model shown in Figure 9-12 is simply a model. Recombination repair is an important mechanism because it eliminates the n
6、ecessity for delaying replication for the many hours that would be needed foe excision repair to remove all thymine dimers. Furthermore, recombination repair may correct some kinds of damage that cannot be corrected by excision repair-for example, alterations that do not cause be helix distortion bu
7、t do stop DNA synthesis. Recombinational repair can also occur with UV-irradiated phages. If a population of a phage that fails to engage in excision repair is UV-irradiated, fewer phage plate on a recA-host than a recA+ host. In contrast to excision repair, recombinational repair occurs after DNA r
8、eplication; hence, recombination repair has been called postreplicational repair. Recombination repair is also called daughter-strand gap repair because only the gaps formed by opposite dimers, rather than the dimers themselves, are repaired.胸腺嘧啶二聚体的修复这个子链有一个大的缺口。这是每个未被切除的胸腺嘧啶二聚体。有一种方法通过单独可持续的复制可以产生
9、可生育的子细胞，因为这个链上的胸腺嘧啶二聚体将持续产生有缺口的子链并且在进入缺口的时候第一组有缺口的子链就会变成碎片。然而，通过重组机制包括姐妹链的交换，产生一条完整的双链。姐妹链的概念就是完整的单链部分是与相对应的DNA片段相分离的并且插入这个缺口产生相对应的胸腺嘧啶二聚体（图9-12）。他的基因重组需要RecA蛋白质。DNA聚合酶I合成补足链，并且DNA连接酶插入到相邻的DNA,因此填补了空缺.。这个有切除物形成的空缺通过DNA聚合酶I和连接酶进行修补的。如果每个胸腺嘧啶二聚体都是通过这种方法修复，形成两个单独完整的子链，并且每一条链都可以在下一个复制循环中作为模板合成对应的另一条链，因为
10、损坏的姐妹链可以利用这一点来重组另一条链。许多分子水平遗传学的重组修复还不被知道，因此图9-12只是个简单的模型。重组修复是一个很重要的机制，因为它消除了延迟复制花费很长时间的需要，这种延迟修复是指切除修复移除所有的胸腺嘧啶二聚体。因此，重组修复可以纠正一些切除修复不能纠正的损伤，例如，改变这些不会导致扭曲螺旋但是完成了DNA的综合体。 重组修复也可以出现在紫外线辐射的噬菌体上。如果一个被紫外线辐射的噬菌体种群不能进行切除修复, 在平板上recA突变型宿主比recA野生型宿主的噬菌体少。与切除修复相比，重组修复出现在DNA复制之后;因此重组修复又叫做postreplicational 修复。重
11、组修复又称作子链缺口的修复，因为只有这个缺口是通过与之对应的二聚体形成的，而不是二聚体自身被修复。2 SOS repair Recall that UV light is a powerful mutagen. The repair processes we have discussed thus far, however, are not mutagenic; photoreactivation, excision repair, and recombinational repairs all result in faithful repair of the damage. A clue t
12、o UV mutagenesis is that an amount of mutagenesis is not a linear function of UV dose: Mutagenesis requires high doses of UV. This finding suggests that when the amount of UV damage (chiefly thymine dimers) exceeds the capacity of the faithful repair systems to correct the DNA damage, another proces
13、s can allow cell survival but at the cost of mutagenesis. This process is called SOS repair(derived from the international distress signal) because it is a “last ditch” attempt to allow DNA replication-and hence cell survival-to proceed. It therefore seems that unrepaired DNA damage somehow induces
14、the SOS response. Thus, SOS repair is a bypass system that allows DNA chain growth across damaged segments at the cost of fidelity of replication. It is an error-prone process; that is, even though intact DNA strands are formed, the strands often contain incorrect bases. SOS repair is not yet thorou
15、ghly understood, but one of the results seems to be a relaxation of the editing system to allow polymerization to proceed across a dimer (transdimer synthesis) despite the distortion of the helix. SOS repair is the major cause of mutagenesis by UV and many chemical mutagens. Regulation of the SOS re
16、sponse The SOS response involves the coordinate turn-on and turn-off of a large number of genes (about 20) following extensive DNA damage. The genetics and physiology of the SOS response were a confusing puzzle until a connection was made between a function of the RecA protein and the induction of phage. Recall that phage has two potential lifestyles: either lytic growth producing infective virus or lysogenic growth integrated into the ch
