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Gibberellins modulate light signaling pathways to prevent Arabidopsis seedling de‐etiolation in darkness
Author(s) -
Alabadí David,
GallegoBartolomé Javier,
Orlando Leonardo,
GarcíaCárcel Laura,
Rubio Vicente,
Martínez Cristina,
Frigerio Martín,
IglesiasPedraz Juan Manuel,
Espinosa Ana,
Deng Xing Wang,
Blázquez Miguel A.
Publication year - 2008
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.2007.03346.x
Subject(s) - photomorphogenesis , hypocotyl , gibberellin , phytochrome , etiolation , arabidopsis , ubiquitin ligase , crosstalk , biology , darkness , microbiology and biotechnology , transcription factor , mutant , signal transduction , phytochrome a , ubiquitin , genetics , botany , biochemistry , gene , physics , optics , enzyme , red light
Summary In many plants, photomorphogenesis is the default developmental program after seed germination, and provides the key features that allow adaptation to light. This program is actively repressed if germination occurs in the absence of light, through a mechanism dependent on the E3 ubiquitin ligase activity that is encoded in Arabidopsis by COP1 ( CO NSTITUTIVE P HOTOMORPHOGENIC 1), which induces proteolytic degradation of transcription factors necessary for light‐regulated development, such as HY5 (LONG HY POCOTYL 5) and HYH (LONG HY POCOTYL 5 H OMOLOG), and stabilization of transcription factors that promote skotomorphogenesis, such as PIF3 ( P HYTOCHROME I NTERACTING F ACTOR 3). Seedlings deficient in gibberellin (GA) synthesis or signaling display a de‐etiolated phenotype when grown in darkness, equivalent to the phenotype of cop1 mutants, which indicates that the switch between photo‐ and skotomorphogenesis is also under hormonal control. Here we provide evidence for the existence of crosstalk between GA and the COP1‐mediated pathway, and identify HY5 and the PIF family as nodes of a regulatory network. This interaction occurs through distinct molecular mechanisms, based on the observation that GA signaling regulates protein stability of HY5, and the activity of PIF3.