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蓝光诱导负调控因子光敏色素互作因子1的降解,以促进拟南芥幼苗的光形态建成发育。

Blue light induces degradation of the negative regulator phytochrome interacting factor 1 to promote photomorphogenic development of Arabidopsis seedlings.

作者信息

Castillon Alicia, Shen Hui, Huq Enamul

机构信息

University of Texas, Austin, Texas 78712, USA.

出版信息

Genetics. 2009 May;182(1):161-71. doi: 10.1534/genetics.108.099887. Epub 2009 Mar 2.

Abstract

Phytochrome interacting factors (PIFs) are nuclear basic helix-loop-helix (bHLH) transcription factors that negatively regulate photomorphogenesis both in the dark and in the light in Arabidopsis. The phytochrome (phy) family of photoreceptors induces the rapid phosphorylation and degradation of PIFs in response to both red and far-red light conditions to promote photomorphogenesis. Although phys have been shown to function under blue light conditions, the roles of PIFs under blue light have not been investigated in detail. Here we show that PIF1 negatively regulates photomorphogenesis at the seedling stage under blue light conditions. pif1 seedlings displayed more open cotyledons and slightly reduced hypocotyl length compared to wild type under diurnal (12 hr light/12 hr dark) blue light conditions. Double-mutant analyses demonstrated that pif1phyA, pif1phyB, pif1cry1, and pif1cry2 have enhanced cotyledon opening compared to the single photoreceptor mutants under diurnal blue light conditions. Blue light induced the rapid phosphorylation, polyubiquitination, and degradation of PIF1 through the ubi/26S proteasomal pathway. PIF1 interacted with phyA and phyB in a blue light-dependent manner, and the interactions with phys are necessary for the blue light-induced degradation of PIF1. phyA played a dominant role under pulses of blue light, while phyA, phyB, and phyD induced the degradation of PIF1 in an additive manner under prolonged continuous blue light conditions. Interestingly, the absence of cry1 and cry2 enhanced the degradation of PIF1 under blue light conditions. Taken together, these data suggest that PIF1 functions as a negative regulator of photomorphogenesis under blue light conditions and that blue light-activated phys induce the degradation of PIF1 through the ubi/26S proteasomal pathway to promote photomorphogenesis.

摘要

光敏色素互作因子(PIFs)是一类核碱性螺旋-环-螺旋(bHLH)转录因子,在拟南芥中,无论是在黑暗还是光照条件下,它们都对光形态建成起负调控作用。光感受器的光敏色素(phy)家族在红光和远红光条件下会诱导PIFs的快速磷酸化和降解,以促进光形态建成。尽管已证明phy在蓝光条件下起作用,但尚未对蓝光条件下PIFs的作用进行详细研究。在此,我们表明PIF1在蓝光条件下对幼苗期的光形态建成起负调控作用。与野生型相比,在昼夜(12小时光照/12小时黑暗)蓝光条件下,pif1幼苗的子叶张开程度更大,下胚轴长度略有缩短。双突变分析表明,与单一光感受器突变体相比,在昼夜蓝光条件下,pif1phyA、pif1phyB、pif1cry1和pif1cry2的子叶张开程度增强。蓝光通过泛素/26S蛋白酶体途径诱导PIF1的快速磷酸化、多聚泛素化和降解。PIF1以蓝光依赖的方式与phyA和phyB相互作用,与phy的相互作用是蓝光诱导PIF1降解所必需的。phyA在蓝光脉冲下起主导作用,而在长时间连续蓝光条件下,phyA、phyB和phyD以累加方式诱导PIF1的降解。有趣的是,cry1和cry2缺失会增强蓝光条件下PIF1的降解。综上所述,这些数据表明PIF1在蓝光条件下作为光形态建成的负调控因子发挥作用,并且蓝光激活的phy通过泛素/26S蛋白酶体途径诱导PIF1的降解以促进光形态建成。

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