拟南芥
生物
根毛
突变体
细胞生物学
转录因子
侧根
内质网
抑制因子
克德尔
分子生物学
基因
生物化学
高尔基体
作者
Diana Rosa Rodríguez-Garcia,Yossmayer del Carmen Rondón Guerrero,Lucía Ferrero,Andrés Hugo Rossi,Esteban A. Miglietta,Ariel Aptekmann,Eliana Marzol,Javier Martínez Pacheco,Mariana Carignani Sardoy,Victoria Berdión Gabarain,Leonel E Lopez,Gabriela Díaz Domínguez,Cecilia Borassi,José J. Sánchez‐Serrano,Lin Xu,Alejandro D. Nadra,Enrique Rojo,Federico Ariel,José M. Estevez
出处
期刊:Plant Physiology
[Oxford University Press]
日期:2023-10-06
卷期号:194 (1): 81-93
标识
DOI:10.1093/plphys/kiad533
摘要
Abstract Plant genomes encode a unique group of papain-type Cysteine EndoPeptidases (CysEPs) containing a KDEL endoplasmic reticulum (ER) retention signal (KDEL-CysEPs or CEPs). CEPs process the cell-wall scaffolding EXTENSIN (EXT) proteins that regulate de novo cell-wall formation and cell expansion. Since CEPs cleave EXTs and EXT-related proteins, acting as cell-wall-weakening agents, they may play a role in cell elongation. The Arabidopsis (Arabidopsis thaliana) genome encodes 3 CEPs (AtCPE1-AtCEP3). Here, we report that the genes encoding these 3 Arabidopsis CEPs are highly expressed in root-hair (RH) cell files. Single mutants have no evident abnormal RH phenotype, but atcep1-3 atcep3-2 and atcep1-3 atcep2-2 double mutants have longer RHs than wild-type (Wt) plants, suggesting that expression of AtCEPs in root trichoblasts restrains polar elongation of the RH. We provide evidence that the transcription factor NAC1 (petunia NAM and Arabidopsis ATAF1, ATAF2, and CUC2) activates AtCEPs expression in roots to limit RH growth. Chromatin immunoprecipitation indicates that NAC1 binds to the promoter of AtCEP1, AtCEP2, and, to a lower extent, AtCEP3 and may directly regulate their expression. Inducible NAC1 overexpression increases AtCEP1 and AtCEP2 transcript levels in roots and leads to reduced RH growth while the loss of function nac1-2 mutation reduces AtCEP1-AtCEP3 gene expression and enhances RH growth. Likewise, expression of a dominant chimeric NAC1-SRDX repressor construct leads to increased RH length. Finally, we show that RH cell walls in the atcep1-3 atcep3-2 double mutant have reduced levels of EXT deposition, suggesting that the defects in RH elongation are linked to alterations in EXT processing and accumulation. Our results support the involvement of AtCEPs in controlling RH polar growth through EXT processing and insolubilization at the cell wall.
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