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A plant plasma-membrane H + -ATPase promotes yeast TORC1 activation via its carboxy-terminal tail
Scientific Reports ( IF 4.6 ) Pub Date : 2021-02-26 , DOI: 10.1038/s41598-021-83525-1
Elie Saliba 1 , Cecilia Primo 1 , Nadia Guarini 1 , Bruno André 1
Affiliation  

The Target of Rapamycin Complex 1 (TORC1) involved in coordination of cell growth and metabolism is highly conserved among eukaryotes. Yet the signals and mechanisms controlling its activity differ among taxa, according to their biological specificities. A common feature of fungal and plant cells, distinguishing them from animal cells, is that their plasma membrane contains a highly abundant H+-ATPase which establishes an electrochemical H+ gradient driving active nutrient transport. We have previously reported that in yeast, nutrient-uptake-coupled H+ influx elicits transient TORC1 activation and that the plasma-membrane H+-ATPase Pma1 plays an important role in this activation, involving more than just establishment of the H+ gradient. We show here that the PMA2 H+-ATPase from the plant Nicotiana plumbaginifolia can substitute for Pma1 in yeast, to promote H+-elicited TORC1 activation. This H+-ATPase is highly similar to Pma1 but has a longer carboxy-terminal tail binding 14–3–3 proteins. We report that a C-terminally truncated PMA2, which remains fully active, fails to promote H+-elicited TORC1 activation. Activation is also impaired when binding of PMA2 to 14–3–3 s is hindered. Our results show that at least some plant plasma-membrane H+-ATPases share with yeast Pma1 the ability to promote TORC1 activation in yeast upon H+-coupled nutrient uptake.



中文翻译:

植物质膜 H + -ATPase 通过其羧基末端尾部促进酵母 TORC1 活化

参与协调细胞生长和代谢的雷帕霉素复合物 1 (TORC1) 的靶标在真核生物中高度保守。然而,根据其生物学特性,控制其活动的信号和机制因分类群而异。真菌和植物细胞的一个共同特征是它们与动物细胞的区别,它们的质膜含有高度丰富的 H + -ATPase,它建立了一个电化学 H +梯度,驱动了主动的营养物质运输。我们之前曾报道过,在酵母中,养分吸收耦合的 H +流入引发瞬时 TORC1 激活,质膜 H + -ATPase Pma1 在此激活中起重要作用,涉及的不仅仅是H + 的建立+渐变。我们在这里展示了来自植物Nicotiana plumbaginifolia的 PMA2 H + -ATPase可以替代酵母中的 Pma1,以促进 H +引发的 TORC1 激活。这种 H + -ATPase 与 Pma1 高度相似,但具有更长的羧基末端尾结合 14-3-3 蛋白质。我们报告说,一个 C 端截断的 PMA2 仍然完全活跃,但不能促进 H +引发的 TORC1 激活。当 PMA2 与 14-3-3 s 的结合受阻时,激活也会受损。我们的结果表明,在至少一些植物等离子体膜H + -ATP酶与酵母PMA1份额促进TORC1激活时ħ酵母的能力+ -偶联的养分吸收。

更新日期:2021-02-26
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