Salicylic acid promotes quiescent center cell division through ROS accumulation and down‐regulation of PLT1, PLT2, and WOX5

分生组织 转录因子 细胞生物学 细胞分裂 突变体 生物 拟南芥 拟南芥 水杨酸 细胞生长 同源盒 NPR1 细胞 基因 遗传学 医学 心力衰竭 内科学 利钠肽
作者
Zhuqing Wang,Duoyan Rong,Dixing Chen,Yang Xiao,Renyi Liu,Shuang Wu,Chizuko Yamamuro
出处
期刊:Journal of Integrative Plant Biology [Wiley]
卷期号:63 (3): 583-596 被引量:52
标识
DOI:10.1111/jipb.13020
摘要

Salicylic acid (SA) plays a crucial role in plant immunity. However, its function in plant development is poorly understood. The quiescent center (QC), which maintains columella stem cells (CSCs) in the root apical meristem and typically exhibits low levels of cell division, is critical for root growth and development. Here, we show that the Arabidopsis thaliana SA overaccumulation mutant constitutively activated cell death 1 (cad1), which exhibits increased cell division in the QC, is rescued by additional mutations in genes encoding the SA biosynthetic enzyme SALICYLIC ACID INDUCTION DEFFICIENT2 (SID2) or the SA receptor NONEXPRESSER OF PR GENES1 (NPR1), indicating that QC cell division in the cad1 mutant is promoted by the NPR1-dependent SA signaling pathway. The application of exogenous SA also promoted QC cell division in wild-type plants in a dose-dependent manner and largely suppressed the expression of genes involved in QC maintenance, including those encoding the APETALA2 (AP2) transcription factors PLETHORA1 (PLT1) and PLT2, as well as the homeodomain transcription factor WUSCHEL-RELATED HOMEOBOX5 (WOX5). Moreover, we showed that SA promotes reactive oxygen species (ROS) production, which is necessary for the QC cell division phenotype in the cad1 mutant. These results provide insight into the function of SA in QC maintenance.
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