AAA-ATPase FIDGETIN-LIKE 1 and Helicase FANCM Antagonize Meiotic Crossovers by Distinct Mechanisms.
AAA-ATPase FIDGETIN-LIKE 1 and Helicase FANCM Antagonize Meiotic Crossovers by Distinct Mechanisms.
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DOI：
10.1371/journal.pgen.1005369
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发表时间：
2015-07
期刊：
影响因子：
4.5
通讯作者：
Mercier R
中科院分区：
文献类型：
--
作者：
Girard C;Chelysheva L;Choinard S;Froger N;Macaisne N;Lemhemdi A;Mazel J;Crismani W;Mercier R
减数分裂交换（COs）产生遗传多样性，对于大多数物种正确完成减数分裂至关重要。它们的发生受到严格限制，但这种限制的机制仍然知之甚少。在此，我们鉴定了保守的AAA-ATPase FIDGETTIN-LIKE-1（FIGL 1）作为减数分裂CO形成的负调节因子。我们表明，拟南芥FIGL 1限制CO形成全基因组，FIGL 1控制两个保守的重组酶DMC 1和RAD 51的动力学和FIGL 1阻碍同源染色体之间的相互作用，这表明FIGL 1抵消DMC 1/RAD 51介导的同源链间入侵，以限制CO的形成。此外，耗尽FIGL 1和先前鉴定的抗CO解旋酶FANCM两者协同地增加交叉频率。此外，我们发现，FANCM突变对重组的影响是低得多的F1杂种自交系的表型相比，而figl 1突变同样增加了在这两种情况下的交叉。这表明FIGL 1和FANCM的作用模式受到基因组背景的不同影响。我们建议，FIGL 1和FANCM代表两个连续的障碍CO形成，一个限制链入侵，其他拆卸D-环，以促进SDSA，当都解除，导致大量增加的交叉，而不损害减数分裂进程。有性繁殖的物种产生的后代在基因上彼此不同，尽管它们有相同的父母。这种独特性是由减数分裂创造的，减数分裂是一种专门的细胞分裂。在减数分裂后，每一个父母都会传递一半的DNA，但每次发生这种情况时，传递给后代的DNA的“半部分”与以前不同。这些差异是由于诉诸父母的染色体，但也重组他们。在这里，我们描述了一个基因-FIDGETIN-LIKE 1-它限制了减数分裂过程中发生的重组量。以前我们发现了一个具有类似功能的基因，FANCM。FIGL 1和FANCM通过不同的机制运作。这一发现将有助于从进化的角度更多地理解为什么重组是自然限制的。这对植物育种也有潜在的重要应用，植物育种主要是对许多“重组体”进行取样，以找到与其亲本相比具有遗传优势的个体。
Meiotic crossovers (COs) generate genetic diversity and are critical for the correct completion of meiosis in most species. Their occurrence is tightly constrained but the mechanisms underlying this limitation remain poorly understood. Here we identified the conserved AAA-ATPase FIDGETIN-LIKE-1 (FIGL1) as a negative regulator of meiotic CO formation. We show that Arabidopsis FIGL1 limits CO formation genome-wide, that FIGL1 controls dynamics of the two conserved recombinases DMC1 and RAD51 and that FIGL1 hinders the interaction between homologous chromosomes, suggesting that FIGL1 counteracts DMC1/RAD51-mediated inter-homologue strand invasion to limit CO formation. Further, depleting both FIGL1 and the previously identified anti-CO helicase FANCM synergistically increases crossover frequency. Additionally, we showed that the effect of mutating FANCM on recombination is much lower in F1 hybrids contrasting from the phenotype of inbred lines, while figl1 mutation equally increases crossovers in both contexts. This shows that the modes of action of FIGL1 and FANCM are differently affected by genomic contexts. We propose that FIGL1 and FANCM represent two successive barriers to CO formation, one limiting strand invasion, the other disassembling D-loops to promote SDSA, which when both lifted, leads to a large increase of crossovers, without impairing meiotic progression. Sexually reproducing species produce offspring that are genetically unique from one another, despite having the same parents. This uniqueness is created by meiosis, which is a specialized cell division. After meiosis each parent transmits half of their DNA, but each time this occurs, the 'half portion' of DNA transmitted to offspring is different from the previous. The differences are due to resorting the parental chromosomes, but also recombining them. Here we describe a gene—FIDGETIN-LIKE 1—which limits the amount of recombination that occurs during meiosis. Previously we identified a gene with a similar function, FANCM. FIGL1 and FANCM operate through distinct mechanisms. This discovery will be useful to understand more, from an evolutionary perspective, why recombination is naturally limited. Also this has potentially significant applications for plant breeding which is largely about sampling many 'recombinants' to find individuals that have heritable advantages compared to their parents.
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ATMUS81在A. thaliana中对干扰不敏感的交叉中的作用。
影响因子：
4.5
作者：
Berchowitz, Luke E.;Francis, Kirk E.;Bey, Alexandra L.;Copenhaver, Gregory P.
通讯作者：
Copenhaver, Gregory P.
DOI：
10.1126/science.1219379
发表时间：
2012-09-07
期刊：
Science (New York, N.Y.)
影响因子：
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作者：
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通讯作者：
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影响因子：
11.6
作者：
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通讯作者：
Bouchez, David
影响因子：
56.9
作者：
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通讯作者：
Mercier, Raphael
影响因子：
14.8
作者：
Berchowitz, Luke E.;Copenhaver, Gregory P.
通讯作者：
Copenhaver, Gregory P.