DNA双链断裂修复缺陷的mus309突变影响黑腹果蝇基因间而非基因内减数分裂重组。

Petter Portin
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引用次数: 11

摘要

研究了黑腹果蝇的次胚性DNA双链断裂修复,特别是合成依赖性链退火和第三染色体缺陷突变mus309对X染色体基因间和基因内减数分裂重组的影响。结果表明,该突变显著增加了所研究的X染色体三个基因间隔中两个基因间杂交的频率。有趣的是,这种增加在X染色体的尖端最为普遍,在这里,每个物理图谱单位长度的交叉通常是最不频繁的。特别是杂交干扰也受到影响,表明mus309突变的影响涉及杂交的前提条件,而不是杂交本身的事件。另一方面,结果也表明,很可能突变对基因内重组,即基因转换没有任何影响。这些结果与目前的减数分裂交叉分子模型完全一致,减数分裂交叉是由DNA双链断裂引发的,随后形成单端入侵中间物或d环,随后加工产生涉及双霍利迪结形成的交叉或非交叉产物。具体而言,研究结果表明mus309基因参与d环的分解,从而影响减数分裂重组中双链断裂修复(DSBR)和合成依赖链退火(SDSA)途径的选择。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
mus309 mutation, defective in DNA double-strand break repair, affects intergenic but not intragenic meiotic recombination in Drosophila melanogaster.

The effect was investigated of the hypomorphic DNA double-strand break repair, notably synthesis-dependent strand annealing, deficient mutation mus309 on the third chromosome of Drosophila melanogaster on intergenic and intragenic meiotic recombination in the X chromosome. The results showed that the mutation significantly increases the frequency of intergenic crossing over in two of three gene intervals of the X chromosome studied. Interestingly the increase was most prevalent in the tip of the X chromosome where crossovers normally are least frequent per physical map unit length. In particular crossing over interference was also affected, indicating that the effect of the mus309 mutation involves preconditions of crossing over but not the event of crossing over itself. On the other hand, the results also show that most probably the mutation does not have any effect on intragenic recombination, i.e. gene conversion. These results are fully consistent with the present molecular models of meiotic crossing over initiated by double-strand breaks of DNA followed by formation of a single-end-invasion intermediate, or D-loop, which is subsequently processed to generate either crossover or non-crossover products involving formation of a double Holliday junction. In particular the results suggest that the mus309 gene is involved in resolution of the D-loop, thereby affecting the choice between double-strand-break repair (DSBR) and synthesis-dependent strand annealing (SDSA) pathways of meiotic recombination.

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