Arabidopsis PCH2 Mediates Meiotic Chromosome Remodeling and Maturation of Crossovers.
Arabidopsis PCH2 Mediates Meiotic Chromosome Remodeling and Maturation of Crossovers.
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DOI：
10.1371/journal.pgen.1005372
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发表时间：
2015-07
期刊：
影响因子：
4.5
通讯作者：
Franklin FC
中科院分区：
文献类型：
--
作者：
Lambing C;Osman K;Nuntasoontorn K;West A;Higgins JD;Copenhaver GP;Yang J;Armstrong SJ;Mechtler K;Roitinger E;Franklin FC
减数分裂染色体由沿环碱基定位的蛋白质轴组织成线性环染色质阵列。轴的程序性重塑发生在减数分裂的前期I。结构照明显微镜(SIM)显示了拟南芥和甘蓝染色体轴的动态变化。我们发现，轴相关蛋白ASY1在受精卵伴随着联会复合体(SC)的形成过程中被耗尽。对Atpch2突变体的研究表明，这需要保守的AAA+ATPase PCH2，它定位于轴重塑的位置。PCH2的丢失导致ASY1不能从轴上耗尽，并影响SC聚合。重组蛋白在Atpch2中的免疫定位表明，早期I期的重组启动和CO指定是正常发生的。证据表明，CO干扰最初在突变体中起作用，但在指定后CO成熟过程中存在缺陷。这导致CO减少，并导致一些同源染色体对之间无法形成CoS，从而在中期I形成单价染色体。遗传分析表明，CO在某些染色体区域的分布也受到影响。总之，这些数据表明，Atpch2中的轴重构缺陷扰乱了Cos的正常图案化形成。在许多真核生物的生殖细胞中，一个称为减数分裂的过程产生单倍体配子。在减数分裂过程中，同源亲本染色体(同源)重组形成交叉(CO)，从而提供遗传变异。共形成产生称为交叉的物理连接，这是准确的同源分离所必需的。CO控制指定重组前体的一个子集，该子集将成熟以在每个同源对之间形成至少一个交叉。重组伴随着广泛的染色体重组。蛋白质轴的形成将每个同系物的姐妹染色单体对组织成相连的线性环状染色质阵列。然后，成对的同系物排列，突触通过一种蛋白质结构--联会复合体(SC)--沿着它们的长度紧密联系在一起。在前期I结束时，SC被分解并完成重组。我们通过分析蛋白质PCH2的作用来研究重组和染色体重塑之间的联系，我们证明了在SC形成过程中，PCH2是染色体轴重塑所必需的。在野生型中，免疫定位显示沿染色体突触区域的轴组件ASY1的轴相关信号耗尽。在没有PCH2的情况下，ASY1信号不会从染色体轴上消失，SC也不会正常形成。尽管染色体重塑的这种缺陷对CO的命名没有明显的影响，但CO的成熟受到干扰，使得每对同源基因至少形成一个CO的情况不再发生。
Meiotic chromosomes are organized into linear looped chromatin arrays by a protein axis localized along the loop-bases. Programmed remodelling of the axis occurs during prophase I of meiosis. Structured illumination microscopy (SIM) has revealed dynamic changes in the chromosome axis in Arabidopsis thaliana and Brassica oleracea. We show that the axis associated protein ASY1 is depleted during zygotene concomitant with synaptonemal complex (SC) formation. Study of an Atpch2 mutant demonstrates this requires the conserved AAA+ ATPase, PCH2, which localizes to the sites of axis remodelling. Loss of PCH2 leads to a failure to deplete ASY1 from the axes and compromizes SC polymerisation. Immunolocalization of recombination proteins in Atpch2 indicates that recombination initiation and CO designation during early prophase I occur normally. Evidence suggests that CO interference is initially functional in the mutant but there is a defect in CO maturation following designation. This leads to a reduction in COs and a failure to form COs between some homologous chromosome pairs leading to univalent chromosomes at metaphase I. Genetic analysis reveals that CO distribution is also affected in some chromosome regions. Together these data indicate that the axis remodelling defect in Atpch2 disrupts normal patterned formation of COs. In the reproductive cells of many eukaryotes, a process called meiosis generates haploid gametes. During meiosis, homologous parental chromosomes (homologs) recombine forming crossovers (CO) that provide genetic variation. CO formation generates physical links called chiasmata, which are essential for accurate homolog segregation. CO control designates a sub-set of recombination precursors that will mature to form at least one chiasma between each homolog pair. Recombination is accompanied by extensive chromosome reorganization. Formation of a proteinaceous axis organizes the pairs of sister chromatids of each homolog into conjoined linear looped chromatin arrays. Pairs of homologs then align and synapse becoming closely associated along their length by a protein structure, the synaptonemal complex (SC). The SC is disassembled at the end of prophase I and recombination is completed. We have investigated the link between recombination and chromosome remodelling by analysing the role of a protein, PCH2, which we show is required for remodelling of the chromosome axis during SC formation. In wild type, immunolocalization reveals depletion of the axis-associated signal of the axis component, ASY1, along synapsed regions of the chromosomes. In the absence of PCH2, the ASY1 signal is not depleted from the chromosome axis and the SC does not form normally. Although this defect in chromosome remodelling has no obvious effect on CO designation, CO maturation is perturbed such that the formation of at least one CO per homolog pair no longer occurs.