Coarsening dynamics can explain meiotic crossover patterning in both the presence and absence of the synaptonemal complex.
Coarsening dynamics can explain meiotic crossover patterning in both the presence and absence of the synaptonemal complex.
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DOI：
10.7554/elife.79408
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发表时间：
2023-02-27
期刊：
影响因子：
7.7
通讯作者：
Howard M
中科院分区：
文献类型：
--
作者：
Fozard JA;Morgan C;Howard M
由减数分裂交换促进的遗传物质的洗牌是遗传变异的关键驱动力。因此，必须仔细控制交叉事件的数量和位置。在拟南芥中，在缺乏联会复合体（SC）（一种保守的蛋白质支架）的突变体中，每个染色体对上的专性交换和附近交换的抑制被废除。我们使用数学建模和定量超分辨率显微镜探索和机械地解释减数分裂交叉模式在拟南芥线完整，不完整，或废除突触。对于zyp1突变体，缺乏SC，我们开发了一个粗化模型，在该模型中，交叉前体全球竞争有限的池的亲交叉因子HEI10，通过核质介导的动态HEI10交换。我们证明，该模型能够定量再现和预测zyp1实验交叉图案和HEI10焦点强度数据。此外，我们发现，一个模型相结合的SC和核质介导的粗化可以解释交叉模式在野生型拟南芥和pch2突变体，显示部分突触。总之，我们的研究结果表明，野生型拟南芥和SC缺陷突变体的交叉模式的调节可能通过相同的基本粗化机制起作用，不同的只是空间隔室通过亲交叉因子扩散。
The shuffling of genetic material facilitated by meiotic crossovers is a critical driver of genetic variation. Therefore, the number and positions of crossover events must be carefully controlled. In Arabidopsis, an obligate crossover and repression of nearby crossovers on each chromosome pair are abolished in mutants that lack the synaptonemal complex (SC), a conserved protein scaffold. We use mathematical modelling and quantitative super-resolution microscopy to explore and mechanistically explain meiotic crossover pattering in Arabidopsis lines with full, incomplete, or abolished synapsis. For zyp1 mutants, which lack an SC, we develop a coarsening model in which crossover precursors globally compete for a limited pool of the pro-crossover factor HEI10, with dynamic HEI10 exchange mediated through the nucleoplasm. We demonstrate that this model is capable of quantitatively reproducing and predicting zyp1 experimental crossover patterning and HEI10 foci intensity data. Additionally, we find that a model combining both SC- and nucleoplasm-mediated coarsening can explain crossover patterning in wild-type Arabidopsis and in pch2 mutants, which display partial synapsis. Together, our results reveal that regulation of crossover patterning in wild-type Arabidopsis and SC-defective mutants likely acts through the same underlying coarsening mechanism, differing only in the spatial compartments through which the pro-crossover factor diffuses.