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脱落酸通过在主要调控因子无口基因上印记一种SnRK2激酶介导的磷酸化编码来调节气孔的产生。

Abscisic acid regulates stomatal production by imprinting a SnRK2 kinase-mediated phosphocode on the master regulator SPEECHLESS.

作者信息

Yang Xin, Gavya S Lalitha, Zhou Zimin, Urano Daisuke, Lau On Sun

机构信息

Department of Biological Sciences, National University of Singapore, 14 Science Drive 4, Singapore 117557, Singapore.

Temasek Life Sciences Laboratory, 1 Research Link, Singapore 117604, Singapore.

出版信息

Sci Adv. 2022 Oct 7;8(40):eadd2063. doi: 10.1126/sciadv.add2063.

Abstract

Stomata, the epidermal pores for gas exchange between plants and the atmosphere, are the major sites of water loss. During water shortage, plants limit the formation of new stoma via the phytohormone abscisic acid (ABA) to conserve water. However, how ABA suppresses stomatal production is largely unknown. Here, we demonstrate that three core SnRK2 kinases of ABA signaling inhibit the initiation and proliferation of the stomatal precursors in . We show that the SnRK2s function within the precursors and directly phosphorylate SPEECHLESS (SPCH), the master transcription factor for stomatal initiation. We identify specific SPCH residues targeted by the SnRK2s, which mediate the ABA/drought-induced suppression of SPCH and stomatal production. This SnRK2-specific SPCH phosphocode connects stomatal development with ABA/drought signals and enables the independent control of this key water conservation response. Our work also highlights how distinct signaling activities can be specifically encoded on a master regulator to modulate developmental plasticity.

摘要

气孔是植物与大气之间进行气体交换的表皮孔,也是水分流失的主要部位。在缺水期间,植物通过植物激素脱落酸(ABA)限制新气孔的形成以保存水分。然而,ABA如何抑制气孔产生在很大程度上尚不清楚。在这里,我们证明ABA信号传导的三种核心SnRK2激酶抑制气孔前体在[具体植物名称未给出]中的起始和增殖。我们表明,SnRK2s在前体中发挥作用,并直接磷酸化气孔起始的主要转录因子无沉默(SPCH)。我们确定了SnRK2s靶向的特定SPCH残基,这些残基介导ABA/干旱诱导的SPCH和气孔产生的抑制。这种SnRK2特异性的SPCH磷酸密码将气孔发育与ABA/干旱信号联系起来,并实现对这种关键的节水反应的独立控制。我们的工作还突出了不同的信号活动如何能够在一个主要调节因子上被特异性编码以调节发育可塑性。

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