Wang JG, Chen CH, Chien CT, Hsieh HL

FAR-RED INSENSITIVE 219 (FIN219) in Arabidopsis is involved in phytochrome A-mediated far-red (FR) light signaling. Previous genetic studies revealed that FIN219 acts as an extragenic suppressor of CONSTITUTIVE PHOTOMORPHOGENIC 1 (COP1). However, the molecular mechanism underlying the suppression of COP1 remains unknown. Here, we used a transgenic approach to study ...

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the regulation of COP1 by FIN219. Transgenic seedlings containing ectopic expression of the FIN219 N-terminal domain in wild-type Columbia (named NCox for the expression of the N-terminal coiled-coil domain and NTox for the N-terminal 300 amino-acid region) exhibited a dominant-negative long-hypocotyl phenotype under FR, reflected as reduced photomorphogenic responses and altered levels of COP1 and HY5. Yeast two-hybrid, pull-down, and bimolecular fluorescence complementation assays revealed that FIN219 could interact with the WD-40 domain of COP1 and with its N-terminal coiled-coil domain through its C-terminal domain. Further in vivo coimmunoprecipitation study confirms that FIN219 interacts with COP1 under continuous FR light. Studies of the double mutant fin219-2/cop1-6 indicated that HY5 stability requires FIN219 under darkness and FR light. Moreover, FIN219 levels positively regulated by phytochrome A can modulate the subcellular location of COP1 and are differentially regulated by various fluence rates of FR light. We concluded that the dominant-negative long-hypocotyl phenotype conferred by NCox and NTox in a wild-type background was caused by the misregulation of COP1 binding with the C terminus of FIN219. Our data provide a critical mechanism controlling the key repressor COP1 in response to FR light.

Date: Apr. 27, 2011

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