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细胞壁完整性受体Mtl1在葡萄糖可用性受损时有助于清晰地调节自噬反应。

The Cell Wall Integrity Receptor Mtl1 Contributes to Articulate Autophagic Responses When Glucose Availability Is Compromised.

作者信息

Montella-Manuel Sandra, Pujol-Carrion Nuria, de la Torre-Ruiz Maria Angeles

机构信息

Cell Signalling in Yeast Unit, Department of Basic Medical Sciences, Institut de Recerca Biomèdica de Lleida (IRBLleida), University of Lleida, 25198 Lleida, Spain.

出版信息

J Fungi (Basel). 2021 Oct 26;7(11):903. doi: 10.3390/jof7110903.

DOI:10.3390/jof7110903
PMID:34829194
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8623553/
Abstract

Mtl1protein is a cell wall receptor belonging to the CWI pathway. Mtl1 function is related to glucose and oxidative stress signaling. In this report, we show data demonstrating that Mtl1 plays a critical role in the detection of a descent in glucose concentration, in order to activate bulk autophagy machinery as a response to nutrient deprivation and to maintain cell survival in starvation conditions. Autophagy is a tightly regulated mechanism involving several signaling pathways. The data here show that in  , Mtl1 signals glucose availability to either Ras2 or Sch9 proteins converging in Atg1 phosphorylation and autophagy induction. TORC1 complex function is not involved in autophagy induction during the diauxic shift when glucose is limited. In this context, the gene is required to regulate autophagy activation upon amino acid starvation independent of the TORC1 complex. Mtl1 function is also involved in signaling the autophagic degradation of mitochondria during the stationary phase through both Ras2 and Sch9, in a manner dependent on either Atg33 and Atg11 proteins and independent of the Atg32 protein, the mitophagy receptor. All of the above suggest a pivotal signaling role for Mtl1 in maintaining correct cell homeostasis function in periods of glucose scarcity in budding yeast.

摘要

Mtl1蛋白是一种属于细胞壁完整性(CWI)途径的细胞壁受体。Mtl1的功能与葡萄糖和氧化应激信号传导有关。在本报告中,我们展示的数据表明,Mtl1在检测葡萄糖浓度下降方面发挥着关键作用,以便激活整体自噬机制,作为对营养剥夺的反应,并在饥饿条件下维持细胞存活。自噬是一种涉及多个信号通路的严格调控机制。此处的数据表明,在……中,Mtl1将葡萄糖可用性信号传递给Ras2或Sch9蛋白,这些信号在Atg1磷酸化和自噬诱导中汇聚。当葡萄糖有限时,TORC1复合体功能不参与在双相转变期间的自噬诱导。在这种情况下,……基因是在氨基酸饥饿时独立于TORC1复合体调节自噬激活所必需的。Mtl1的功能还涉及在稳定期通过Ras2和Sch9以依赖于Atg33和Atg11蛋白且独立于线粒体自噬受体Atg32蛋白的方式,向线粒体的自噬降解发出信号。上述所有情况表明,Mtl1在芽殖酵母葡萄糖缺乏时期维持正确的细胞稳态功能中起着关键的信号传导作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe42/8623553/5a0b6d4771e3/jof-07-00903-g008a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe42/8623553/7aa29e31f0ad/jof-07-00903-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe42/8623553/03d468c8e086/jof-07-00903-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe42/8623553/5a3ef97aa471/jof-07-00903-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe42/8623553/45efab6fb246/jof-07-00903-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe42/8623553/a56302338b08/jof-07-00903-g005a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe42/8623553/79c462ae190b/jof-07-00903-g006a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe42/8623553/2c70f4d9a587/jof-07-00903-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe42/8623553/5a0b6d4771e3/jof-07-00903-g008a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe42/8623553/7aa29e31f0ad/jof-07-00903-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe42/8623553/03d468c8e086/jof-07-00903-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe42/8623553/5a3ef97aa471/jof-07-00903-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe42/8623553/45efab6fb246/jof-07-00903-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe42/8623553/a56302338b08/jof-07-00903-g005a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe42/8623553/79c462ae190b/jof-07-00903-g006a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe42/8623553/2c70f4d9a587/jof-07-00903-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe42/8623553/5a0b6d4771e3/jof-07-00903-g008a.jpg

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