下胚轴
拟南芥
生物
细胞生物学
延伸率
拟南芥
微管
转录因子
植物
突变体
生物化学
基因
材料科学
极限抗拉强度
冶金
作者
Dingding Zhou,Xiaohong Wang,Xiangfeng Wang,Tonglin Mao
出处
期刊:The Plant Cell
[Oxford University Press]
日期:2023-02-14
卷期号:35 (6): 2044-2061
被引量:4
标识
DOI:10.1093/plcell/koad042
摘要
Hypocotyl elongation is an important morphological response during plant thermomorphogenesis. Multiple studies indicate that the transcription factor PHYTOCHROME-INTERACTING FACTOR 4 (PIF4) is a key regulator of high temperature-induced hypocotyl elongation. However, the underlying cellular mechanisms regarding PIF4-mediated hypocotyl elongation are largely unclear. In this study, we found that PIF4 regulates the PLANT U-BOX TYPE E3 UBIQUITIN LIGASE 31 (PUB31)-SPIRAL1 (SPR1) module and alters cortical microtubule reorganization to promote hypocotyl cell elongation during Arabidopsis thaliana (Arabidopsis) thermomorphogenesis. SPR1 loss-of-function mutants exhibit much shorter hypocotyls when grown at 28 °C, indicating a positive role for SPR1 in high ambient temperature-induced hypocotyl elongation. High ambient temperature induces SPR1 expression in a PIF4-dependent manner, and stabilizes SPR1 protein to mediate microtubule reorganization. Further investigation showed that PUB31 interacts with and ubiquitinates SPR1. In particular, the ubiquitinated effect on SPR1 was moderately decreased at high temperature, which was due to the direct binding of PIF4 to the PUB31 promoter and down-regulating its expression. Thus, this study reveals a mechanism in which PIF4 induces SPR1 expression and suppresses PUB31 expression, resulting in the accumulation and stabilization of SPR1 protein, and further promoting hypocotyl cell elongation by altering cortical microtubule organization during Arabidopsis thermomorphogenesis.
科研通智能强力驱动
Strongly Powered by AbleSci AI