避光
光敏色素
拟南芥
向光性
突变体
茉莉酸
下胚轴
生物
细胞生物学
调节器
转录因子
植物
光形态发生
叶柄(昆虫解剖学)
远红色
蓝光
红灯
遗传学
水杨酸
基因
物理
膜翅目
光学
作者
Maite Saura-Sánchez,Tai Sabrina Chiriotto,Jimena Cascales,Gabriel Gómez‐Ocampo,Jorge Hernández‐García,Zheng Li,José L. Pruneda-Paz,Miguel Á. Blázquez,Javier Francisco Botto
出处
期刊:Plant and Cell Physiology
[Oxford University Press]
日期:2023-01-27
卷期号:64 (5): 474-485
被引量:6
摘要
Abstract Shade avoidance syndrome (SAS) is a strategy of major adaptive significance and typically includes elongation of the stem and petiole, leaf hyponasty, reduced branching and phototropic orientation of the plant shoot toward canopy gaps. Both cryptochrome 1 and phytochrome B (phyB) are the major photoreceptors that sense the reduction in the blue light fluence rate and the low red:far-red ratio, respectively, and both light signals are associated with plant density and the resource reallocation when SAS responses are triggered. The B-box (BBX)-containing zinc finger transcription factor BBX24 has been implicated in the SAS as a regulator of DELLA activity, but this interaction does not explain all the observed BBX24-dependent regulation in shade light. Here, through a combination of transcriptional meta-analysis and large-scale identification of BBX24-interacting transcription factors, we found that JAZ3, a jasmonic acid signaling component, is a direct target of BBX24. Furthermore, we demonstrated that joint loss of BBX24 and JAZ3 function causes insensitivity to DELLA accumulation, and the defective shade-induced elongation in this mutant is rescued by loss of DELLA or phyB function. Therefore, we propose that JAZ3 is part of the regulatory network that controls the plant growth in response to shade, through a mechanism in which BBX24 and JAZ3 jointly regulate DELLA activity. Our results provide new insights into the participation of BBX24 and JA signaling in the hypocotyl shade avoidance response in Arabidopsis.
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