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酵母Lsm促凋亡突变体在自噬方面表现出缺陷。

Yeast Lsm Pro-Apoptotic Mutants Show Defects in Autophagy.

作者信息

Caraba Benedetta, Stirpe Mariarita, Palermo Vanessa, Vaccher Ugo, Bianchi Michele Maria, Falcone Claudio, Mazzoni Cristina

机构信息

Department of Biology and Biotechnologies "C. Darwin", Sapienza University of Rome, Piazzale Aldo Moro 5, 00185 Roma, Italy.

出版信息

Int J Mol Sci. 2023 Sep 5;24(18):13708. doi: 10.3390/ijms241813708.

DOI:10.3390/ijms241813708
PMID:37762007
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10530990/
Abstract

is an essential yeast gene encoding a component of different LSM complexes involved in the regulation of mRNA splicing, stability, and translation. In previous papers, we reported that the expression in of the gene lacking the C-terminal Q/N-rich domain in an null strain () restored cell viability. Nevertheless, in this transformed strain, we observed some phenotypes that are typical markers of regulated cell death, reactive oxygen species (ROS), and oxidated RNA accumulation. In this paper, we report that a similar truncation operated in the gene confers on cells the same phenotypes observed with the gene. Up until now, there was no evidence of the direct involvement of in autophagy. Here we found that the mutant showed a block in the autophagic process and was very sensitive to nitrogen starvation or treatment with low doses of rapamycin, an inducer of autophagy. Moreover, both during nitrogen starvation and aging, the mutant accumulated cytoplasmic autophagy-related structures, suggesting a role of Lsm4 in a later step of the autophagy process.

摘要

是一个重要的酵母基因,编码参与mRNA剪接、稳定性和翻译调控的不同LSM复合物的一个组分。在之前的论文中,我们报道了在一个缺失菌株()中缺乏C末端富含Q/N结构域的基因的表达恢复了细胞活力。然而,在这个转化菌株中,我们观察到了一些受调控细胞死亡、活性氧(ROS)和氧化RNA积累的典型标志物的表型。在本文中,我们报道在基因中进行的类似截短赋予细胞与基因观察到的相同表型。到目前为止,没有证据表明直接参与自噬。在这里我们发现突变体在自噬过程中出现阻滞,并且对氮饥饿或低剂量雷帕霉素(一种自噬诱导剂)处理非常敏感。此外,在氮饥饿和衰老过程中,突变体都积累了细胞质自噬相关结构,表明Lsm4在自噬过程的后期步骤中发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5799/10530990/a4a6cb83254d/ijms-24-13708-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5799/10530990/608c72c187ea/ijms-24-13708-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5799/10530990/81645b478065/ijms-24-13708-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5799/10530990/e76987a922d9/ijms-24-13708-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5799/10530990/a4a6cb83254d/ijms-24-13708-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5799/10530990/608c72c187ea/ijms-24-13708-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5799/10530990/81645b478065/ijms-24-13708-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5799/10530990/e76987a922d9/ijms-24-13708-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5799/10530990/a4a6cb83254d/ijms-24-13708-g004.jpg

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