State Key Laboratory of Genetic Engineering and Ministry of Education Key Laboratory of Biodiversity Sciences and Ecological Engineering, Institute of Plant Biology, School of Life Sciences, Fudan University, Shanghai 200438, China.
Department of Biology and Integrative Program for Biological and Genome Sciences, University of North Carolina, Chapel Hill, North Carolina 27599-3280.
Plant Physiol. 2019 Feb;179(2):446-459. doi: 10.1104/pp.18.00861. Epub 2018 Nov 20.
Meiotic recombination contributes to the maintenance of the association between homologous chromosomes (homologs) and ensures the accurate segregation of homologs during anaphase I, thus facilitating the redistribution of alleles among progeny. Meiotic recombination is initiated by the programmed formation of DNA double strand breaks, the repair of which requires DNA synthesis, but the role of DNA synthesis proteins during meiosis is largely unknown. Here, we hypothesized that the lagging strand-specific DNA Polymerase δ (POL δ) might be required for meiotic recombination, based on a previous analysis of DNA Replication Factor1 that suggested a role for lagging strand synthesis in meiotic recombination. In Arabidopsis (), complete mutation of the catalytic subunit of POL δ, encoded by , leads to embryo lethality. Therefore, we used a meiocyte-specific knockdown strategy to test this hypothesis. Reduced expression of in meiocytes caused decreased fertility and meiotic defects, including incomplete synapsis, the formation of multivalents, chromosome fragmentation, and improper segregation. Analysis of meiotic crossover (CO) frequencies showed that plants had significantly fewer interference-sensitive COs than the wild type, indicating that AtPOL δ participates in type I CO formation. double mutant meiocytes displayed more severe meiotic phenotypes than those of either single mutant, suggesting that the function of AtPOLD1 and AtPOL2A is not identical in meiotic recombination. Given that POL δ is highly conserved among eukaryotes, we hypothesize that the described role of POL δ here in meiotic recombination likely exists widely in eukaryotes.
减数分裂重组有助于维持同源染色体(同源物)之间的联系,并确保在后期 I 中同源物的准确分离,从而促进等位基因在后代中的重新分配。减数分裂重组是由 DNA 双链断裂的程序性形成引发的,其修复需要 DNA 合成,但 DNA 合成蛋白在减数分裂中的作用在很大程度上是未知的。在这里,我们假设基于先前对 DNA 复制因子 1 的分析,滞后链特异性 DNA 聚合酶 δ(POL δ)可能是减数分裂重组所必需的,该分析表明滞后链合成在减数分裂重组中起作用。在拟南芥()中,POL δ 的催化亚基(由编码)的完全突变导致胚胎致死。因此,我们使用减数分裂细胞特异性敲低策略来检验这一假设。在减数分裂细胞中表达的减少导致生育力下降和减数分裂缺陷,包括不完全联会、多价体的形成、染色体碎片化和不当分离。分析减数分裂交叉(CO)频率表明,植物的干涉敏感 CO 比野生型明显减少,表明 AtPOL δ 参与了 I 型 CO 的形成。AtPOL δ 双突变体减数分裂细胞的减数分裂表型比任一单突变体更为严重,表明 AtPOLD1 和 AtPOL2A 的功能在减数分裂重组中并不相同。鉴于 POL δ 在真核生物中高度保守,我们假设这里描述的 POL δ 在减数分裂重组中的作用可能在真核生物中广泛存在。