Plants undergo contrasting developmental programs in dark and light. Photomorphogenesis, a light-adapted programme is repressed in the dark by the synergistic actions of CUL4(COP1-SPA) E3 ubiquitin ligase and a subset of basic helix-loop-helix transcription factors called phytochrome interacting factors (PIFs). To promote photomorphogenesis, light activates the phytochrome family of sensory photoreceptors, which inhibits these repressors by poorly understood mechanisms. Here, we show that the CUL4(COP1-SPA) E3 ubiquitin ligase is necessary for the light-induced degradation of PIF1 in Arabidopsis. The light-induced ubiquitylation and subsequent degradation of PIF1 is reduced in the cop1, spaQ and cul4 backgrounds. COP1, SPA1 and CUL4 preferentially form complexes with the phosphorylated forms of PIF1 in response to light. The cop1 and spaQ seeds display strong hyposensitive response to far-red light-mediated seed germination and light-regulated gene expression. These data show a mechanism by which an E3 ligase attenuates its activity by degrading its cofactor in response to light.

中文翻译：

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CUL4与COP1和SPA形成E3连接酶，以促进光诱导的PIF1降解。

植物在黑暗和光明中经历相反的发育程序。通过在CUL4（COP1-SPA）E3泛素连接酶和称为植物色素相互作用因子（PIFs）的基本螺旋-环-螺旋转录因子的子集的协同作用下，在黑暗中抑制了光形态发生，一种适应光的程序。为了促进光形态发生，光激活了感觉光感受器的植物色素家族，通过知之甚少的机制抑制了这​​些阻遏物。在这里，我们表明，CUL4（COP1-SPA）E3泛素连接酶对于拟南芥中光诱导的PIF1降解是必需的。在cop1，spaQ和cul4背景下，光诱导的PIF1泛素化和随后的降解降低。响应光，COP1，SPA1和CUL4优先与PIF1的磷酸化形式形成复合物。cop1和spaQ种子对远红光介导的种子萌发和光调节基因表达表现出强烈的过敏反应。这些数据显示了一种机制，通过这种机制，E3连接酶可通过响应光降解其辅因子来减弱其活性。