Plants undergo postembryonic growth during the developmental transition from germinating seeds to seedlings. Recent studies suggest LEAFY COTYLEDON1 (LEC1), initially identified as a central regulator in embryogenesis and seed maturation in Arabidopsis thaliana, plays a distinct role in postembryonic development. However, the mechanism by which LEC1 regulates nonembryonic development still remains elusive. In this study, we observed etiolation-related phenotypes in early seedlings of lec1 mutants and inducible LEC1 overexpression transgenic lines. Consistent with this, LEC1 promotes the expression of hypocotyl elongation-related genes in a darkness-dependent manner in spite of the comparable LEC1 transcript levels in the light- and dark-grown seedlings. Furthermore, we show that LEC1 interacts with PHYTOCHROME-INTERACTING FACTOR4 (PIF4), a major transcription modulator in postgermination development, to interdependently regulate hypocotyl elongation-related genes via direct binding to G-box element in the dark. Moreover, loss of LEC1 function suppresses the elongated hypocotyl phenotype of PIF-overaccumulating plants; conversely, inducible overexpression of LEC1 does not rescue the short hypocotyl in pif4 mutants. Our findings reveal that LEC1 acts as a coactivator of PIFs in transcriptional regulation during postembryonic growth, providing a possible mechanism by which plants fine-tune morphological development for their survival during the transition from the embryonic phase to seedling establishment.
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