TOR and SnRK1 fine tune SPEECHLESS transcription and protein stability to optimize stomatal development in response to exogenously supplied sugar
TOR and SnRK1 fine tune SPEECHLESS transcription and protein stability to optimize stomatal development in response to exogenously supplied sugar
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TOR 和 SnRK1 微调 SPEECHLESS 转录和蛋白质稳定性，以优化气孔发育以响应外源供应的糖
DOI：
10.1111/nph.17984
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发表时间：
2022-02-08
期刊：
影响因子：
9.4
通讯作者：
Bai, Ming-Yi
中科院分区：
文献类型：
--
作者：
Han, Chao;Qiao, Yan;Bai, Ming-Yi
在拟南芥中，表皮细胞向气孔的分化受到内源和环境信号的调控。糖是植物表皮细胞增殖和分化所必需的。然而，目前还不清楚表皮细胞如何维持分裂和分化，以产生适当数量的气孔，以响应不同的糖供应。在这里，我们表明，两个进化上保守的激酶Snf 1相关的蛋白激酶1（SnRK 1）和雷帕霉素的目标（TOR）发挥关键作用，在调节气孔发育不同的糖供应。当植物生长在含有1%蔗糖的培养基上时，蔗糖激活的TOR通过诱导气孔发育的主调节因子SPEECHLESS（SPCH）的表达来促进气孔发育。SnRK 1通过磷酸化和稳定SPCH促进气孔发育。然而，在高糖条件下，大量积累的海藻糖-6-磷酸（Tre 6P）通过降低SnRK 1的催化α亚基KIN 10与其上游激酶的相互作用，抑制了KIN 10的活性，从而促进了SPCH的降解，抑制了气孔发育。我们的研究结果表明，TOR和SnRK 1精细调节SPCH的表达和蛋白质的稳定性，以优化气孔发育响应外源糖。
In Arabidopsis, the differentiation of epidermal cells into stomata is regulated by endogenous and environmental signals. Sugar is required for plant epidermal cell proliferation and differentiation. However, it is unclear how epidermal cells maintain division and differentiation to generate proper amounts of stomata in response to different sugar availability. Here, we show that two evolutionarily conserved kinase Snf1-related protein kinase 1 (SnRK1) and Target of rapamycin (TOR) play critical roles in the regulation of stomatal development under different sugar availability. When plants are grown on a medium containing 1% sucrose, sucrose-activated TOR promotes the stomatal development by inducing the expression of SPEECHLESS (SPCH), a master regulator of stomatal development. SnRK1 promotes stomatal development through phosphorylating and stabilizing SPCH. However, under the high sucrose conditions, the highly accumulated trehalose-6-phosphate (Tre6P) represses the activity of KIN10, the catalytic alpha-subunit of SnRK1, by reducing the interaction between KIN10 and its upstream kinase, consequently promoting SPCH degradation and inhibiting stomatal development. Our findings revealed that TOR and SnRK1 finely regulate SPCH expression and protein stability to optimize the stomatal development in response to exogenously supplied sugar.