Abstract
Cytokinin is a plant hormone regulating numerous biological processes. Its diverse functions are realized through the expression control of specific target genes. The transcription of the immediate early cytokinin target genes is regulated by type-B response regulator proteins (RRBs), which are transcription factors (TFs) of the Myb family. RRB activity is controlled by phosphorylation and protein degradation. Here, we focus on another step of regulation, the interaction of RRBs among each other or with other TFs to form active or repressive TF complexes. Several examples in Arabidopsis thaliana illustrate that RRBs form homodimers or complexes with other TFs to specify the cytokinin response. This increases the variability of the output response and provides opportunities of crosstalk between the cytokinin signaling pathway and other cellular signaling pathways. We propose that a targeted approach is required to uncover the full extent and impact of RRB interaction with other TFs.
Highlights
The plant hormone cytokinin has numerous biological activities in regulating plant development and biotic and abiotic stress responses [1,2,3]
The former case is illustrated by the influence of DELLAs and several other transcription factors (TFs) on developmental processes regulated by RRBs, while for the latter case, two examples describe that RRBs modulate the activity of BASIC REGION/LEUCINE ZIPPER (bZIP) in the response to different stresses
RRBs, the cytokinin output TFs, are likewise able to interact with other TFs belonging to different families, including the AP2/ERF family members CYTOKININ RESPONSE FACTOR (CRF), the bZIPs TGA1A-RELATED GENE 3 (TGA3) and bZIP63, DELLAs and SQUAMOSA PROMOTER BINDING PROTEIN-LIKE (SPL) to regulate and specify the transcriptional output of cytokinin signaling (Table 1)
Summary
The plant hormone cytokinin has numerous biological activities in regulating plant development and biotic and abiotic stress responses [1,2,3]. Despite genome-wide coverage of gene expression data it is largely unknown how the context-dependent specificity of the transcriptional response to CK is achieved. A small family of F-box proteins, the KISS ME DEADLY (KMD) protein family, interact with RRBs to target them for proteasomal degradation [61] In this way, KMD proteins act as negative regulators of the cytokinin response. In this review we will give an overview on yet another possibility to regulate the transcriptional output of the cytokinin signal, namely RRB dimerization or complex formation with other TFs to diversify the cytokinin output
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