胚胎致死性突变zyg-10(b261)是atx-2基因的一个等位基因,破坏了早期胚胎发生的多个方面。

microPublication biology Pub Date : 2025-08-28 eCollection Date: 2025-01-01 DOI:10.17912/micropub.biology.001714
Zachary G Bell, Harold E Smith, Kevin F O'Connell
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引用次数: 0

摘要

在对秀丽隐杆线虫温度敏感的胚胎致死性突变的早期筛选中,发现了zyg-10 (b261)突变,但胚胎致死性表型背后的细胞学缺陷以及zyg-10的分子身份此前尚未确定。本研究表明,zyg-10 (b261)是atx-2基因的等位基因,由atx-2 (b261)母体产生的胚胎表现出多种缺陷,包括卵壳缺陷、细胞质分裂失败、纺锤体错位和染色体分离错误。我们还发现,在atx-2 (b261)胚胎中,作为蛋壳形成和有丝分裂调节因子的分离酶的定位存在缺陷。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

The embryonic lethal mutation <i>zyg-10(b261)</i> is an allele of the <i>atx-2</i> gene and disrupts multiple aspects of early embryogenesis.

The embryonic lethal mutation zyg-10(b261) is an allele of the atx-2 gene and disrupts multiple aspects of early embryogenesis.

The zyg-10 ( b261 ) mutation was identified in one of the earliest screens for temperature-sensitive embryonic lethal mutations in C. elegans , but the cytological defects underlying the embryonic lethal phenotype, as well as the molecular identity of zyg-10 had not been previously established. Here we show that zyg-10 ( b261 ) is an allele of the atx-2 (ataxin-related) gene and that embryos produced by atx-2 ( b261 ) mothers exhibit a variety of defects including eggshell defects, cytokinesis failure, spindle mispositioning, and chromosome missegregation. We also show that the localization of separase, a regulator of egg-shell formation and mitosis, is defective in atx-2 ( b261 ) embryos.

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