内质网和核内膜泛素结合酶Ubc6和Ubc7赋予酿酒酵母对土霉素B的抗性

microPublication biology Pub Date : 2024-07-29 eCollection Date: 2024-01-01 DOI:10.17912/micropub.biology.001276

Sophia L Owutey, Katrina A Procuniar, Emmanuel Akoto, Jacob C Davis, Rachel M Vachon, LiLi F O'Malley, Hayden O Schneider, Philip J Smaldino, Jason D True, Ashley L Kalinski, Eric M Rubenstein

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摘要

异常的内质网（ER）和核内膜（INM）蛋白通过ER相关降解（ERAD）和INM相关降解（INMAD）被破坏。我们之前研究发现，酿酒酵母中的 Hrd1、Doa10 和 Asi ERAD 和 INMAD 泛素连接酶（E3s）可赋予酿酒酵母对土霉素 B 的抗性，而土霉素 B 会扭曲核糖体解码中心。在这里，我们评估了 Ubc6 和 Ubc7（主要的 ERAD 和 INMAD 泛素连接酶（E2s））对土霉素 B 抗性的要求。缺失任何一种E2都会使细胞对百菌清B过敏，而缺失UBC7的影响更大，这与Ubc6和Ubc7在ER和INM蛋白质量控制中的作用一致。

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Endoplasmic reticulum and inner nuclear membrane ubiquitin-conjugating enzymes Ubc6 and Ubc7 confer resistance to hygromycin B in Saccharomyces cerevisiae.

Aberrant endoplasmic reticulum (ER) and inner nuclear membrane (INM) proteins are destroyed through ER-associated degradation (ERAD) and INM-associated degradation (INMAD). We previously showed the Hrd1, Doa10, and Asi ERAD and INMAD ubiquitin ligases (E3s) in Saccharomyces cerevisiae confer resistance to hygromycin B, which distorts the ribosome decoding center. Here, we assessed the requirement of Ubc6 and Ubc7, the primary ERAD and INMAD ubiquitin-conjugating enzymes (E2s) for hygromycin B resistance. Loss of either E2 sensitized cells to hygromycin B, with UBC7 deletion having a greater impact, consistent with characterized roles for Ubc6 and Ubc7 in ER and INM protein quality control.

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