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SUMO-mediated regulation of synaptonemal complex formation during meiosis

机译:SUMO介导的减数分裂过程中突触复合物形成的调控

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摘要

The propagation of most sexually reproducing species is possible due to a specialized form of cell division known as meiosis, which leads to the formation of haploid gametes that fuse upon fertilization, reconstituting the species ploidy. A hallmark of meiosis is the ability to segregate homologous chromosomes away from each other, thereby reducing the chromosome set by half. Mechanistically, this involves pairing, synapsis, and the reciprocal exchange of genetic material (crossover recombination) between homologous chromosomes during prophase I. These events ensure that homologs remain physically connected even after they desynapse, allowing for their proper alignment at the metaphase plate and subsequent segregation to opposite poles of the spindle during the first meiotic division. Failures in ho-molog recognition or in maintaining homologous interactions invariably disrupt meiotic segregation and result in aneuploid gametes. The importance of proper homologous segregation is underscored by the infertility, miscarriages, and various birth defects that trace back to errors in single meiotic events in the paternal or maternal germline progenitors (Hassold and Hunt 2001)
机译:由于称为减数分裂的特殊细胞分裂形式,大多数有性繁殖物种的繁殖是可能的,这导致单倍体配子的形成,这些单倍体配子受精后融合,从而使物种倍性恢复。减数分裂的标志是能够将同源染色体彼此分离,从而将染色体组减少一半。从机制上讲,这涉及配对,突触和在前期I期间同源染色体之间遗传物质的相互交换(交叉重组)。​​这些事件可确保同源物即使在去突触后仍保持物理连接,从而使其在中期板和随后的序列中正确对齐在第一次减数分裂过程中分离到纺锤体的相反两极。同源识别失败或无法保持同源相互作用均会破坏减数分裂分离并导致非整倍体配子。不育,流产和各种先天缺陷可追溯到正确的同源隔离的重要性,这些缺陷可追溯到父系或母系生殖系祖先的单个减数分裂事件中的错误(Hassold和Hunt 2001)。

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