SPEECHLESS integrates brassinosteroid and stomata signalling pathways
SPEECHLESS integrates brassinosteroid and stomata signalling pathways
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DOI：
10.1038/ncb2471
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发表时间：
2012-05-01
影响因子：
21.3
通讯作者：
Russinova, Eugenia
中科院分区：
文献类型：
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作者：
Gudesblat, Gustavo E.;Schneider-Pizon, Joanna;Russinova, Eugenia
气孔形成受多种发育和环境信号的调节，但这些信号如何整合以控制这一过程尚未完全了解（1）。在拟南芥中，碱性螺旋-环-螺旋转录因子SPEECHLESS（SPCH）调节气孔谱系发育过程中发生的进入、扩增和间隔分裂。SPCH活性受丝裂原活化蛋白激酶（MAPK）介导的磷酸化负调控（2）。在这里，我们表明，除了MAPKs，SPCH活动也调制油菜素类固醇（BR）信号。GSK 3/SHAGGY样激酶BIN 2（BR INSENSITIVE 2）磷酸化与MAPK靶向残基重叠的残基，以及MAPK靶结构域外蛋白质氨基末端区域的四个残基。这些磷酸化事件拮抗SPCH活性并限制表皮细胞增殖。相反，在体内抑制BIN 2活性稳定SPCH，并引发过多的气孔和非气孔细胞的形成。我们证明，通过磷酸化输入从MAPKs和BIN 2，SPCH作为一个整合节点的气孔和BR信号通路，以控制拟南芥气孔发育。
Stomatal formation is regulated by multiple developmental and environmental signals, but how these signals are integrated to control this process is not fully understood(1). In Arabidopsis thaliana, the basic helix-loop-helix transcription factor SPEECHLESS (SPCH) regulates the entry, amplifying and spacing divisions that occur during stomatal lineage development. SPCH activity is negatively regulated by mitogen-activated protein kinase (MAPK)-mediated phosphorylation(2). Here, we show that in addition to MAPKs, SPCH activity is also modulated by brassinosteroid (BR) signalling. The GSK3/SHAGGY-like kinase BIN2 (BR INSENSITIVE2) phosphorylates residues overlapping those targeted by the MAPKs, as well as four residues in the amino-terminal region of the protein outside the MAPK target domain. These phosphorylation events antagonize SPCH activity and limit epidermal cell proliferation. Conversely, inhibition of BIN2 activity in vivo stabilizes SPCH and triggers excessive stomatal and non-stomatal cell formation. We demonstrate that through phosphorylation inputs from both MAPKs and BIN2, SPCH serves as an integration node for stomata and BR signalling pathways to control stomatal development in Arabidopsis.