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镉诱导热带假丝酵母 3Aer 中 GAPDH 和 MDH 介导的延迟细胞衰老和功能障碍。

Cadmium induces GAPDH- and- MDH mediated delayed cell aging and dysfunction in Candida tropicalis 3Aer.

机构信息

University Institute of Medical Laboratory Technology (UIMLT), Faculty of Allied Health Sciences (FAHS), The University of Lahore, Lahore, Pakistan.

Department of Microbiology, Government College University Faisalabad (GCUF), Jhang Road, Faisalabad, Pakistan.

出版信息

Environ Monit Assess. 2019 Jul 11;191(8):490. doi: 10.1007/s10661-019-7631-9.

DOI:10.1007/s10661-019-7631-9
PMID:31297613
Abstract

Eukaryotes employ various mechanisms to survive environmental stress conditions. Multicellular organisms eliminate permanently damaged cells by apoptosis, while unicellular eukaryotes like yeast react by decelerating cell aging. In the present study, transcriptomic and proteomic approaches were employed to elucidate the underlying mechanism of delayed apoptosis. Our findings suggest that Candida tropicalis 3Aer has a set of tightly controlled genes that are activated under Cd exposition. Acute exposure to Cd halts the cell cycle at the G/M phase checkpoint and activates multiple cytoplasmic proteins that overcome effects of Cd-induced reactive oxygen species. Prolonged Cd stress damages DNA and initiates GAPDH amyloid formation. This is the first report that Cd challenge initiates dynamic redistribution of GAPDH and MDH and alters various metabolic pathways including the pentose phosphate pathway. In conclusion, the intracellular redistribution of GAPDH and MDH induced by prolonged cadmium stress modulates various cellular reactions, which facilitate delayed aging in the yeast cell.

摘要

真核生物采用多种机制来应对环境胁迫条件。多细胞生物通过细胞凋亡清除永久性受损细胞,而酵母等单细胞真核生物则通过减缓细胞衰老来做出反应。在本研究中,采用转录组学和蛋白质组学方法阐明了延迟细胞凋亡的潜在机制。我们的研究结果表明,热带假丝酵母 3Aer 具有一组受严格控制的基因,这些基因在 Cd 暴露下被激活。急性 Cd 暴露会使细胞周期在 G/M 期检查点停滞,并激活多种细胞质蛋白,从而克服 Cd 诱导的活性氧的影响。长期 Cd 应激会损害 DNA 并引发 GAPDH 淀粉样蛋白的形成。这是首次报道 Cd 胁迫会引发 GAPDH 和 MDH 的动态重分布,并改变包括戊糖磷酸途径在内的各种代谢途径。总之,长期镉胁迫诱导的 GAPDH 和 MDH 在细胞内的重新分布调节了各种细胞反应,从而促进了酵母细胞的延迟衰老。

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