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嘌呤霉素敏感氨基肽酶PAM-1的缺失在第一次有丝分裂期间触发纺锤体组装检查点。

Loss of the puromycin-sensitive aminopeptidase, PAM-1, triggers the spindle assembly checkpoint during the first mitotic division in .

作者信息

Durkan Aidan, Koup Annalise, Bell Sarah E, Lyczak Rebecca

机构信息

Biology, Ursinus College, Collegeville, Pennsylvania, United States.

出版信息

MicroPubl Biol. 2024 Apr 2;2024. doi: 10.17912/micropub.biology.001167. eCollection 2024.

DOI:10.17912/micropub.biology.001167
PMID:38633870
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11022077/
Abstract

Puromycin-sensitive aminopeptidases have long been implicated in cell-cycle regulation, but the mechanism remains unknown. Here we show that mutations in the gene encoding the puromycin-sensitive aminopeptidase, PAM-1 , cause chromosome segregation defects and an elongated mitosis in the one-cell embryo. Depleting a known regulator of the spindle assembly checkpoint (SAC), MDF-2 (MAD2 in humans), restores normal mitotic timing to mutants but exacerbates the chromosome segregation defects. Thus, PAM-1 is required for proper attachment of chromosomes to the mitotic spindle and its absence triggers the SAC.

摘要

嘌呤霉素敏感氨基肽酶长期以来一直被认为与细胞周期调控有关，但其机制仍然未知。在此我们表明，编码嘌呤霉素敏感氨基肽酶PAM-1的基因突变会导致单细胞胚胎出现染色体分离缺陷和有丝分裂延长。耗尽纺锤体组装检查点（SAC）的已知调节因子MDF-2（人类中的MAD2）可使突变体的有丝分裂时间恢复正常，但会加剧染色体分离缺陷。因此，PAM-1是染色体正确附着于有丝分裂纺锤体所必需的，缺乏PAM-1会触发SAC。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64ed/11022077/6f69912bd25a/25789430-2024-micropub.biology.001167.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64ed/11022077/6f69912bd25a/25789430-2024-micropub.biology.001167.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64ed/11022077/6f69912bd25a/25789430-2024-micropub.biology.001167.jpg

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本文引用的文献

1
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G3 (Bethesda). 2021 Apr 15;11(4). doi: 10.1093/g3journal/jkab063.
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