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

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...

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Bibliographic Details
Published in:Protoplasma 2017, Vol.254 (1), p.597-601
Main Authors: Wallmeroth, Niklas, Anastasia, Anna Katharina, Harter, Klaus, Berendzen, Kenneth Wayne, Mira-Rodado, Virtudes
Format: Article
Language:English
Subjects:
Arabidopsis - drug effects
Arabidopsis - genetics
Arabidopsis Proteins - genetics
Arabidopsis Proteins - metabolism
Biomedical and Life Sciences
Cell Biology
Cytokinins - pharmacology
Gene Expression Regulation, Plant - drug effects
Genes, Plant
Life Sciences
Plant Sciences
Short Communication
Signal Transduction - drug effects
Signal Transduction - genetics
Transcription, Genetic - drug effects
Zoology
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Summary: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.
ISSN:0033-183X
1615-6102
DOI:10.1007/s00709-016-0944-4