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A Tobacco Calcium-Dependent Protein Kinase, CDPK1, Regulates the Transcription Factor REPRESSION OF SHOOT GROWTH in Response to Gibberellins

机译:烟草钙依赖性蛋白激酶CDPK1调节响应赤霉素表达的生长的转录因子表达。

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摘要

The homeostasis of gibberellins (GAs) is maintained by negative feedback in plants. REPRESSION OF SHOOT GROWTH (RSG) is a tobacco (Nicotiana tabacum) transcriptional activator that has been suggested to play a role in GA feedback by the regulation of GA biosynthetic enzymes. The 14-3-3 signaling proteins negatively regulate RSG by sequestering it in the cytoplasm in response to GAs. The phosphorylation on Ser-114 of RSG is essential for 14-3-3 binding of RSG. Here, we identified tobacco Ca2+-dependent protein kinase (CDPK1) as an RSG kinase that promotes 14-3-3 binding to RSG by phosphorylation of Ser-114 of RSG. CDPK1 interacts with RSG in a Ca2+-dependent manner in vivo and in vitro and specifically phosphorylates Ser-114 of RSG. Inhibition of CDPK repressed the GA-induced phosphorylation of Ser-114 of RSG and the GA-induced nuclear export of RSG. Overexpression of CDPK1 inhibited the feedback regulation of a GA 20-oxidase gene and resulted in sensitization to the GA biosynthetic inhibitor. Our results suggest that CDPK1 decodes the Ca2+ signal produced by GAs and regulates the intracellular localization of RSG.
机译:赤霉素(GAs)的稳态通过植物中的负反馈得以维持。抑制生长(RSG)是一种烟草(Nicotiana tabacum)转录激活因子,已被证明可通过调节GA生物合成酶在GA反馈中发挥作用。 14-3-3信号蛋白通过响应GAs将RSG隔离在细胞质中,从而负面调节RSG。 RSG的Ser-114上的磷酸化对于RSG的14-3-3结合至关重要。在这里,我们确定了烟草Ca2 +依赖性蛋白激酶(CDPK1)为RSG激酶,通过RSG的Ser-114磷酸化促进与RSG的14-3-3结合。 CDPK1在体内和体外均以Ca2 +依赖性方式与RSG相互作用,并特异性磷酸化RSG的Ser-114。 CDPK的抑制抑制了GA诱导的RSG的Ser-114磷酸化和GA诱导的RSG的核输出。 CDPK1的过表达抑制了GA 20氧化酶基因的反馈调节,并导致对GA生物合成抑制剂的敏感性。我们的结果表明CDPK1解码GAs产生的Ca2 +信号并调节RSG的细胞内定位。

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