PIFs 和 phyB 在光照和逆境反應中可調控轉譯作用之研究

Abstract

在阿拉伯芥中，phytochrome B (phyB)主要感應光和溫度的訊號並透過其活化態Pfr 和非活 化 態 Pr 之間的相互轉換來調節植物中的各種形態發生。 PHYTOCHROME INTERACTING FACTORs (PIFs)是一群可以和 phyB 交互作用的bHLH 轉錄因子，其主要在 phyB 訊號路徑中扮演負向調控者的角色。先前已有研究指出，光照會促進轉譯作用，因而誘導光型態發生。此外，光照所促進的轉譯作用是透過光接受體、E3 黏合酶–COP1、植物激素–生長素、target of rapamycin (TOR)和 ribosomal proteinS6 (RPS6) 組成的光訊息傳遞路徑所共同調控的。然而，phyB或 PIFs 是否參與在轉譯作用的調控仍然未知。在本研究中，我們發現 PIFs 和 phyB也會影響轉譯作用的效率，並參與在光照所調控的 TOR-RPS6 路徑中。相對於野生型白化苗，pifQ 突變株在黑暗下的轉譯作用較強，而 phyB-9 突變株則較弱。此外，PIFs 在黑暗下會抑制 S6K 和 RPS6 的磷酸化，而 phyB 則會促進它們的磷酸化。對於 pifQ 突變株中有較旺盛的光型態發生及轉譯作用現象，生長素的參與可能是必須的。我們發現 PIFs 可以促進對鹽逆境的耐受性，而 phyB 卻會負調控對鹽逆境的耐受性。透過轉錄和轉譯層次的表現分析，我們發現 PIFs 也許是透過抑制總體的轉譯作用和增強特定與逆境調節有關的 mRNA 的轉譯作用，使得植株有更好的逆境耐受性。總結來說， PIFs 和 phyB 可以共同調控轉譯作用來影響光反應和逆境反應。

In Arabidopsis, the photoreceptor phytochrome B (phyB) senses light and temperature cues, which leads to the modulation of essential morphogenic processes in plants by switching between its active Pfr and inactive Pr forms. PHYTOCHROME INTERACTING FACTORs (PIFs) are bHLH transcription factors which interact with phyB and play negative roles in phytochrome signaling pathways. Previous reports showed that light triggers global translation enhancement during photomorphogenesis. Moreover, this light-enhanced translation is coordinated through a light sensing and signaling pathway consisting of photoreceptors, the E3 ligase – CONSTITUTIVE PHOTOMORPHOGENIC 1 (COP1), the phytohormone – auxin, target of rapamycin (TOR), and ribosomal proteinS6 (RPS6). However, whether phyB or PIFs are involved in the translational regulation is still unknown. In this study, we have demonstrated that PIFs and phyB also affect translation efficiency and participate in TOR-RPS6 pathway. Compared to wild-type etiolated seedlings, polysome loading was increased in pifQ mutant and reduced in phyB-9 mutant under dark condition. Moreover, PIFs repress S6K and RPS6 phosphorylation, whereas phyB promotes their phosphorylation. Auxin is necessary for the enhanced photomorphogenesis and probably translation enhancement in pifQ mutants. We also discovered that PIFs promote salt stress tolerance, whereas phyB plays a negative role in salt stress tolerance. Using transcriptional and translational expression analyses, we have shown that PIFs regulate not only general translational repression but also translational enhancement of specific mRNAs under stress condition. Taken together, we hope to reveal the molecular mechanism which PIFs and phyB regulate translation in response to light and stress.