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.

Keywords: Arabidopsis, competitive inhibition, KIDARI (KDR), light signaling, LONG HYPOCOTYL IN FAR-RED 1 (HFR1), PHYTOCHROMEINTERACTING
FACTOR (PIF)