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首页> 外文期刊>Cell cycle >Phylogenetic conservation of the preapoptotic calreticulin exposure pathway from yeast to mammals.
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Phylogenetic conservation of the preapoptotic calreticulin exposure pathway from yeast to mammals.

机译：从酵母菌到哺乳动物的凋亡前钙网蛋白暴露途径的系统发育保护。

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摘要

The pre-apoptotic exposure of calreticulin (CRT) on the cell surface determines the efficient engulfment of mouse or human tumor cells by antigen-presenting dendritic cells. CRT exposure is rapidly induced by anthracyclins and ionizing irradiation and follows a complex signal transduction pathway that is interrupted by depletion of PERK, caspase-8, BAP31, Bax, Bak or SNAREs, as well as by knock-in mutation of eIF2alpha (to make it non-phosphorylable by PERK) or BAP31 (to render it uncleavable by caspase-8). Here, we show that yeast (Saccharomyces cerevisiae) can expose the CRT orthologue CNE1 on the surface in response to cell death induced by the anthracylin mitoxantrone (MTX). This MTX-triggered CNE1 translocation is abolished by knockout of the yeast orthologues of PERK (Gcn2), BAP31 (Yet3) and SNAREs (Nyv1, Sso1). Altogether, our data point to the existence of an ancestral and cell death-related CRT exposure pathway with conserved elements shared between unicellular fungi and mammals.
机译：钙网蛋白（CRT）在细胞表面的凋亡前暴露决定了抗原呈递树突状细胞有效吞噬小鼠或人类肿瘤细胞。 CRT暴露是由蒽环素和电离辐射快速诱导的，并遵循复杂的信号传导途径，该途径被PERK，caspase-8，BAP31，Bax，Bak或SNARE的耗竭以及eIF2alpha的敲入突变所中断（使它不能被PERK磷酸化）或BAP31（使其不能被caspase-8切割）。在这里，我们显示酵母（Saccharomyces cerevisiae）可以响应蒽环霉素米托蒽醌（MTX）诱导的细胞死亡而在表面暴露CRT直向同源物CNE1。通过敲除PERK（Gcn2），BAP31（Yet3）和SNARE（Nyv1，Sso1）的酵母直向同源物，取消了这种MTX触发的CNE1易位。总而言之，我们的数据指出存在祖先和细胞死亡相关的CRT暴露途径，在单细胞真菌和哺乳动物之间共享保守元素。

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