A competitive peptide inhibitor KIDARI negatively regulates HFR1 by forming nonfunctional heterodimers in Arabidopsis photomorphogenesis
Dynamic dimer formation is an elaborate means of modulating transcription factor activities in diverse cellular processes. The basic helix-loop-helix (bHLH) transcription factor LONG HYPOCOTYL IN FAR-RED 1 (HFR1), for example, plays a role in plant photomorphogenesis by forming non-DNA binding heter...
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Published in: | Molecules and cells Vol. 35; no. 1; pp. 25 - 31 |
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Main Authors: | , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Springer
Korean Society for Molecular and Cellular Biology
01-01-2013
Korea Society for Molecular and Cellular Biology |
Subjects: | |
Online Access: | Get full text |
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Summary: | Dynamic dimer formation is an elaborate means of modulating transcription factor activities in diverse cellular processes. The basic helix-loop-helix (bHLH) transcription factor LONG HYPOCOTYL IN FAR-RED 1 (HFR1), for example, plays a role in plant photomorphogenesis by forming non-DNA binding heterodimers with PHYTOCHROMEINTERACTING FACTORS (PIFs). Recent studies have shown that a small HLH protein KIDARI (KDR) negatively regulates the HFR1 activity in the process. However, molecular mechanisms underlying the KDR control of the HFR1 activity are unknown. Here, we demonstrate that KDR attenuates the HFR1 activity by competitively forming nonfunctional heterodimers, causing liberation of PIF4 from the transcriptionally inactive HFR1-PIF4 complex. Accordingly, the photomorphogenic hypocotyl growth of the
HFR1
-overexpres-sing plants can be suppressed by KDR coexpression, as observed in the
HFR1
-deficient
hfr1-201
mutant. These results indicate that the PIF4 activity is modulated through a double layer of competitive inhibition by HFR1 and KDR, which could in turn ensure fine-tuning of the PIF4 activity under fluctuating light conditions. |
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Bibliography: | These authors contributed equally to this work. |
ISSN: | 1016-8478 0219-1032 |
DOI: | 10.1007/s10059-013-2159-2 |