Lehrstuhl für Botanik, Center of Life and Food Sciences Weihenstephan, Technische Universitaet Muenchen, Freising, Germany.
Cell Biology and Plant Biochemistry, Biochemie-Zentrum Regensburg, University of Regensburg, Regensburg, Germany.
PLoS One. 2018 Dec 21;13(12):e0209407. doi: 10.1371/journal.pone.0209407. eCollection 2018.
Plants encode a unique group of papain-type cysteine endopeptidases (CysEP) characterized by a C-terminal KDEL endoplasmic reticulum retention signal (KDEL-CysEP) and an unusually broad substrate specificity. The three Arabidopsis KDEL-CysEPs (AtCEP1, AtCEP2, and AtCEP3) are differentially expressed in vegetative and generative tissues undergoing programmed cell death (PCD). While KDEL-CysEPs have been shown to be implicated in the collapse of tissues during PCD, roles of these peptidases in processes other than PCD are unknown. Using mCherry-AtCEP2 and EGFP-AtCEP1 reporter proteins in wild type versus atcep2 or atcep1 mutant plants, we explored the participation of AtCEP in young root development. Loss of AtCEP2, but not AtCEP1 resulted in shorter primary roots due to a decrease in cell length in the lateral root (LR) cap, and impairs extension of primary root epidermis cells such as trichoblasts in the elongation zone. AtCEP2 was localized to root cap corpses adherent to epidermal cells in the rapid elongation zone. AtCEP1 and AtCEP2 are expressed in root epidermis cells that are separated for LR emergence. Loss of AtCEP1 or AtCEP2 caused delayed emergence of LR primordia. KDEL-CysEPs might be involved in developmental tissue remodeling by supporting cell wall elongation and cell separation.
植物编码了一组独特的木瓜蛋白酶型半胱氨酸内肽酶（CysEP），其特征是具有 C 末端 KDEL 内质网保留信号（KDEL-CysEP）和异常广泛的底物特异性。三种拟南芥 KDEL-CysEPs（AtCEP1、AtCEP2 和 AtCEP3）在经历程序性细胞死亡（PCD）的营养和生殖组织中差异表达。虽然 KDEL-CysEPs 已被证明与 PCD 期间组织崩溃有关，但这些肽酶在 PCD 以外的过程中的作用尚不清楚。我们使用 mCherry-AtCEP2 和 EGFP-AtCEP1 报告蛋白在野生型与 atcep2 或 atcep1 突变体植物中的表达，探索了 AtCEP 在幼根发育中的参与情况。由于侧根（LR）帽中的细胞长度减少，AtCEP2 的缺失而不是 AtCEP1 的缺失导致初生根变短，并且初级根表皮细胞如伸长区中的毛原细胞的延伸受到损害。AtCEP2 定位于与快速伸长区表皮细胞附着的根冠尸体。AtCEP1 和 AtCEP2 在分离用于 LR 出现的根表皮细胞中表达。AtCEP1 或 AtCEP2 的缺失导致 LR 原基的出现延迟。KDEL-CysEPs 可能通过支持细胞壁伸长和细胞分离参与发育组织重塑。
