ArticleProtoplasma2017
Arabidopsis response regulator 22 inhibits cytokinin-regulated gene transcription in vivo.
Article in Protoplasma, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Non-Canonical Inter-Protein Interactions of Key Proteins Belonging to Cytokinin Signaling Pathways.Plants (Basel, Switzerland) · 2025Review
- Article
- Exploring the Binding Affinity of the ARR2 GARP DNA Binding Domain via Comparative Methods.Genes · 2023Article
- Engineering chloroplast development in rice through cell-specific control of endogenous genetic circuits.Plant biotechnology journal · 2021Article
- The Interaction Network and Signaling Specificity of Two-Component System inInternational journal of molecular sciences · 2020Review
- Cytokinin Signaling Downstream of the His-Asp Phosphorelay Network: Cytokinin-Regulated Genes and Their Functions.Frontiers in plant science · 2020Review
- New Insights into Multistep-Phosphorelay (MSP)/ Two-Component System (TCS) Regulation: Are Plants and Bacteria that Different?Plants (Basel, Switzerland) · 2019Review
- Proteomic analysis of the rice (Oryza officinalis) provides clues on molecular tagging of proteins for brown planthopper resistance.BMC plant biology · 2019Article
- Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.