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Reciprocal proteasome-mediated degradation of PIFs and HFR1 underlies photomorphogenic development in Arabidopsis

机译:互惠蛋白酶体介导的PIF和HFR1的降解拟南芥中的光学发育

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摘要

The phytochrome-mediated regulation of photomorphogenesis under red and far-red light conditions involves both positively and negatively acting factors. The positively acting factors (e.g. HY5/HFR1/LAF1 and others) are degraded in the dark to prevent photomorphogenesis. By contrast, the negatively acting factors (e.g. phytochromeinteracting factors or PIFs) are degraded in response to light to promote photomorphogenesis. Here, we show that the negatively acting factor PIF1 is also degraded in the dark by direct heterodimerization with the positively acting factor HFR1. Conversely, PIF1 also promotes the degradation of HFR1 in darkness. PIF1 enhances the poly-ubiquitylation of HFR1 by COP1 in vivo and in vitro. In addition, the reciprocal co-degradation of PIF1 and HFR1 is dependent on the 26S proteasome pathway in vivo. Genetic evidence shows that the hfr1 mutant partially suppresses the constitutive photomorphogenic phenotypes of cop1-6 pif1 and of the quadruple mutant pifq both in the dark and in far-red light conditions. Taken together, these data uncover a co-degradation mechanism between PIFs and HFR1 that underlies photomorphogenic development in Arabidopsis thaliana.
机译:在红色和远红条件下的植物介导的光膀胱调节涉及正面和负面的因子。积极作用因子(例如Hy5 / HFR1 / LaF1等)在黑暗中降解以防止光学发生。相反,响应于光以促进光致血管发生而降解了负作用因子(例如,植物色度偶然因子或PIFS)。这里,我们表明,通过用正极的作用因子HFR1直接异二聚合,在黑暗中也降低了负作用因子PIF1。相反,PIF1还促进了黑暗中HFR1的降解。 PIF1在体内和体外增强COP1的HFR1的聚菌质。此外,PIF1和HFR1的倒常数共分解取决于体内26s蛋白酶体途径。遗传证据表明,HFR1突变体部分抑制COP1-6PIF1的组成型光学表型,并在黑暗和远红光条件下抑制了COP1-6 PIF1的组成显色表型和四重突变PIFQ。总之,这些数据揭示了PIF和HFR1之间的共分解机制,拟南芥在拟南芥中提出了光学发育。

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