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通过过氧化氢和过氧化物酶感知光线。

Light-sensing via hydrogen peroxide and a peroxiredoxin.

机构信息

Department of Chemistry and Molecular Biology, University of Gothenburg, Box 462, S-413 90 Göteborg, Sweden.

Department of Physics, Chalmers University of Technology, S-412 96 Göteborg, Sweden.

出版信息

Nat Commun. 2017 Mar 24;8:14791. doi: 10.1038/ncomms14791.

DOI:10.1038/ncomms14791
PMID:28337980
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5376668/
Abstract

Yeast lacks dedicated photoreceptors; however, blue light still causes pronounced oscillations of the transcription factor Msn2 into and out of the nucleus. Here we show that this poorly understood phenomenon is initiated by a peroxisomal oxidase, which converts light into a hydrogen peroxide (HO) signal that is sensed by the peroxiredoxin Tsa1 and transduced to thioredoxin, to counteract PKA-dependent Msn2 phosphorylation. Upon HO, the nuclear retention of PKA catalytic subunits, which contributes to delayed Msn2 nuclear concentration, is antagonized in a Tsa1-dependent manner. Conversely, peroxiredoxin hyperoxidation interrupts the HO signal and drives Msn2 oscillations by superimposing on PKA feedback regulation. Our data identify a mechanism by which light could be sensed in all cells lacking dedicated photoreceptors. In particular, the use of HO as a second messenger in signalling is common to Msn2 oscillations and to light-induced entrainment of circadian rhythms and suggests conserved roles for peroxiredoxins in endogenous rhythms.

摘要

酵母缺乏专门的光感受器;然而,蓝光仍然导致转录因子 Msn2 明显地进出细胞核的振荡。在这里,我们表明,这种理解甚少的现象是由过氧化物酶体氧化酶引发的,该氧化酶将光转化为过氧化氢(HO)信号,该信号被过氧化物还原酶 Tsa1 感知,并转导至硫氧还蛋白,以抵消 PKA 依赖性 Msn2 磷酸化。在 HO 的情况下,核保留 PKA 催化亚基,这有助于延迟 Msn2 核浓度,以 Tsa1 依赖性方式拮抗。相反,过氧化物还原酶的超氧化中断了 HO 信号,并通过叠加 PKA 反馈调节来驱动 Msn2 振荡。我们的数据确定了一种机制,通过该机制,所有缺乏专门光感受器的细胞都可以感知光。特别是,HO 作为信号转导中的第二信使,在 Msn2 振荡以及光诱导的生物钟节律同步中很常见,这表明过氧化物还原酶在内源性节律中具有保守作用。

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