The Rim15-endosulfine-PP2ACdc55 signalling module regulates entry into gametogenesis and quiescence via distinct mechanisms in budding yeast.
The Rim15-endosulfine-PP2ACdc55 signalling module regulates entry into gametogenesis and quiescence via distinct mechanisms in budding yeast.
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DOI：
10.1371/journal.pgen.1004456
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发表时间：
2014-06
期刊：
影响因子：
4.5
通讯作者：
Arumugam P
中科院分区：
文献类型：
--
作者：
Sarkar S;Dalgaard JZ;Millar JB;Arumugam P
休眠和配子发生是芽殖酵母在营养饥饿条件下的两种不同的生存策略。酵母细胞如何精确地感知环境信号以触发静止和配子发生还没有完全理解。一个保守的信号传导模块，由长城激酶，硫丹和蛋白磷酸酶PP 2ACdc 55蛋白调节进入有丝分裂在非洲爪蟾卵提取物和减数分裂成熟的苍蝇。我们在这里报告说，一个类似的信号模块组成的丝氨酸-苏氨酸激酶Rim 15，内砜Igo 1和Igo 2和蛋白磷酸酶PP 2ACdc 55，调节进入休眠和配子发生在芽殖酵母。PP 2ACdc 55抑制进入配子发生和静止。Rim 15通过在保守的丝氨酸残基磷酸化将Igo 1转化为PP 2ACdc 55的抑制剂，促进进入配子发生和静止。此外，我们表明，Rim 15-Endosulfine-PP 2ACdc 55途径调节进入静止期和配子发生不同的机制。此外，我们发现Igo 1和Igo 2是减数分裂前自噬所必需的，但减数分裂前自噬的缺乏不足以解释Igo 1 Δ Igo 2 Δ细胞的孢子形成缺陷。我们建议，Rim 15-Endosulfine-PP 2ACdc 55信号模块触发进入静止和配子发生通过调节不同的底物的去磷酸化。细胞的基本属性是感知环境的变化，然后以最大化其生存机会的方式做出反应。当二倍体芽殖酵母细胞受到完全营养饥饿时，它们有两种可能的命运，即静止和配子发生。静止细胞具有降低的转录和翻译速率和增加的应激耐受性。配子发生导致产生可以长期存活的单倍体孢子。在本文中，我们报告了一个信号模块，调节进入休眠和配子发生在芽殖酵母。该模块由三个分子组分组成，即丝氨酸-苏氨酸激酶Rim 15，磷酸酶PP 2ACdc 55和称为endosulfine的保守蛋白。PP 2ACdc 55负调控进入配子发生和静止。在营养饥饿时，Rim 15变得活跃并磷酸化硫丹。这将内硫素转化为PP 2ACdc 55的抑制剂，从而导致进入静止期和配子发生。值得注意的是，由长城激酶、PP 2A-B55 δ和硫丹组成的类似模块调节青蛙卵提取物中进入有丝分裂和苍蝇中的减数分裂成熟，表明该信号传导模块在进化过程中高度保守并被增选以控制不同生物体中的不同生物过程。
Quiescence and gametogenesis represent two distinct survival strategies in response to nutrient starvation in budding yeast. Precisely how environmental signals are sensed by yeast cells to trigger quiescence and gametogenesis is not fully understood. A conserved signalling module consisting of Greatwall kinase, Endosulfine and Protein Phosphatase PP2ACdc55 proteins regulates entry into mitosis in Xenopus egg extracts and meiotic maturation in flies. We report here that an analogous signalling module consisting of the serine-threonine kinase Rim15, the Endosulfines Igo1 and Igo2 and the Protein Phosphatase PP2ACdc55, regulates entry into both quiescence and gametogenesis in budding yeast. PP2ACdc55 inhibits entry into gametogenesis and quiescence. Rim15 promotes entry into gametogenesis and quiescence by converting Igo1 into an inhibitor of PP2ACdc55 by phosphorylating at a conserved serine residue. Moreover, we show that the Rim15-Endosulfine-PP2ACdc55 pathway regulates entry into quiescence and gametogenesis by distinct mechanisms. In addition, we show that Igo1 and Igo2 are required for pre-meiotic autophagy but the lack of pre-meiotic autophagy is insufficient to explain the sporulation defect of igo1Δ igo2Δ cells. We propose that the Rim15-Endosulfine-PP2ACdc55 signalling module triggers entry into quiescence and gametogenesis by regulating dephosphorylation of distinct substrates. The fundamental property of a cell is to sense changes in the environment and then respond in a way that maximizes its chances of survival. When diploid budding yeast cells are subjected to complete nutrient starvation they have two possible fates, namely quiescence and gametogenesis. Quiescent cells have reduced rates of transcription and translation and increased stress tolerance. Gametogenesis results in production of haploid spores that can survive for long periods of time. In this paper, we report a signalling module that regulates entry into both quiescence and gametogenesis in budding yeast. The module consists of three molecular components namely a serine-threonine kinase Rim15, a phosphatase PP2ACdc55 and a conserved protein called as endosulfine. PP2ACdc55 negatively regulates entry into gametogenesis and quiescence. Upon nutrient starvation, Rim15 becomes active and phosphorylates endosulfine. This converts endosulfine to an inhibitor of PP2ACdc55 and thereby leading to entry into quiescence and gametogenesis. Remarkably, an analogous module consisting of Greatwall kinase, PP2A-B55δ and endosulfine regulates entry into mitosis in frog egg extracts and meiotic maturation in flies suggesting that this signalling module is highly conserved and co-opted during evolution to control distinct biological processes in different organisms.
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