Arabidopsis response regulator 22 inhibits cytokinin-regulated gene transcription in vivo

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• 作者：Niklas Wallmeroth ; Anna Katharina Anastasia ; Klaus Harter…
• 关键词：TCS ; Cytokinin ; ARR22 ; ARR5 ; Phosphatase
• 刊名：Protoplasma
• 出版年：2017
• 出版时间：January 2017
• 年：2017
• 卷：254
• 期：1
• 页码：597-601
• 全文大小：
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Cell Biology; Plant Sciences; Zoology;
• 出版者：Springer Vienna
• ISSN：1615-6102
• 卷排序：254

文摘

Cytokinin signaling in Arabidopsis is carried out by a two-component system (TCS) multi-step phosphorelay mechanism that involves three different protein families: histidine kinases (AHKs), phosphotransfer proteins (AHPs), and response regulators (ARRs) that are in turn, subdivided into A-, B- and C-type ARRs depending on their function and structure. Upon cytokinin perception, AHK proteins autophosphorylate; this phosphate is then transferred from the AHKs to the AHPs to finally reach the ARRs. When B-type ARRs are activated by phosphorylation, they function as transcription factors that regulate the expression of cytokinin-dependent genes such as the A-type ARRs, among many others. In cytokinin signaling, while A- and B-type ARR function is well understood, it is still unclear if C-type ARRs (ARR22 and ARR24) play a role in this mechanism. Here, we describe a novel method suitable to study TCS activity natively as an in vivo system. We also show that ARR22 inhibits gene transcription of an A-type ARR upon cytokinin treatment in vivo. Consequently, we propose that ARR22, by acting as a phosphatase on specific AHPs, disrupts the TCS phosphorelay and prevents B-type ARR phosphorylation, and thus their activation as transcription factors, explaining the observed deactivation of cytokinin-responsive genes.