Dev Cell|四川大学生科院在BR和光信号精细调控叶绿体发育机制研究取得新进展

拟南芥糖原合酶激酶3（GSK3）样激酶在植物发育中扮演各种角色， 包括叶绿体的发育，但潜在的分子机制尚不清楚。 本研究，我们证明转录因子GLK1和GLK2与BRASSINOSTEROID insensitive2（BIN2）相互作用并被其磷酸化。 BIN2及其同系物bin2-3 bil1 bil2的功能丧失突变体， 显示出异常的叶绿体发育，而功能获得突变体bin2-1对BR诱导的脱绿不敏感，每粒颗粒类囊体数量减少，表明BIN2正调控着叶绿体的发育。

此外，BIN2在T175，T238，T248和T175处磷酸化GLK1。 T256和这些磷酸化位点的突变会改变GLK1蛋白质的稳定性和DNA结合并损害 植物对BR /黑暗的反应。

另一方面，BR和黑暗会抑制BIN2-GLK模块 增强BR /黑暗介导的脱绿作用，并损害光合装置的形成。 因此，我们的结果提供了BR调节光形态发生和叶绿体发育的机制。

Arabidopsis GLYCOGEN SYNTHASE KINASE 3 (GSK3)-like kinases play various roles in plant development, including chloroplast development, but the underlying molecular mechanism is not well defined. Here, we demonstrate that transcription factors GLK1 and GLK2 interact with and are phosphorylated by the BRASSINOSTEROID insensitive2 (BIN2). The loss-of-function mutant of BIN2 and its homologs, bin2-3 bil1 bil2, displays abnormal chloroplast development, whereas the gain-of-function mutant, bin2-1, exhibits insensitivity to BR-induced de-greening and reduced numbers of thylakoids per granum, suggesting that BIN2 positively regulates chloroplast development. Furthermore, BIN2 phosphorylates GLK1 at T175, T238, T248, and T256, and mutations of these phosphorylation sites alter GLK1 protein stability and DNA binding and impair plant responses to BRs/darkness. On the other hand, BRs and darkness repress the BIN2-GLK module to enhance BR/dark-mediated de-greening and impair the formation of the photosynthetic apparatus. Our results thus provide a mechanism by which BRs modulate photomorphogenesis and chloroplast development.

原文链接：

https://www.cell.com/developmental-cell/pdf/S1534-5807(20)30976-X.pdf

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