Lack of endoplasmic reticulum quality control (ERQC) promotes tonoplast (TP) targeting of KORRIGAN 1 (KOR1).
Lack of endoplasmic reticulum quality control (ERQC) promotes tonoplast (TP) targeting of KORRIGAN 1 (KOR1).
复制标题
内质网质量控制 (ERQC) 的缺乏会促进液泡膜 (TP) 靶向 KORRIGAN 1 (KOR1)。
DOI：
10.1080/15592324.2020.1744348
复制
发表时间：
2020
影响因子：
2.9
通讯作者：
Koiwa,Hisashi
中科院分区：
文献类型：
--
作者：
Nagashima,Yukihiro;Ma,Zeyang;Zhang,Xiuren;vonSchaewen,Antje;Koiwa,Hisashi
KORIGAN 1（KOR 1）的细胞动力学与纤维素合成和植物渗透胁迫耐受性密切相关。KOR 1在质膜（PM）和高尔基体网络（TGN）之间的循环是由细胞转运和质量控制机制识别的序列基序和蛋白质结构维持的。KOR 1的几个突变，以及在宿主遗传背景中，促进KOR 1的错误启动并诱导KOR 1在液泡膜（TP）中的积累。然而，很少有人知道如何保留和排序的KOR 1在PM-TGN循环的调节。对GFP-KOR 1错误定位表型的正向遗传筛选产生了几个具有不同GFP-KOR 1定位模式或信号强度的突变株系。其中一个突变体在尿苷二磷酸葡萄糖：糖蛋白葡萄糖基转移酶（UGGT）位点被破坏，该位点对ER中蛋白质的质量控制至关重要。我们的发现表明KOR 1的错误/未折叠结构触发TP靶向。
Cellular dynamics of KORRIGAN 1 (KOR1) is closely linked with cellulose biosynthesis and plant osmotic stress tolerance. Cycling of KOR1 between the plasma membrane (PM) andtrans-Golgi Network (TGN) is maintained by sequence motifs and protein structures that are recognized by cellular transport and quality control mechanisms. Several mutations in KOR1, as well as in the host genetic background, promote the mistargeting of KOR1 and induce KOR1 accumulation in the tonoplast (TP). Yet, little is known about how retention and sorting of KOR1 are regulated in the PM-TGN cycle. Forward genetic screening for GFP-KOR1 mislocalizing phenotype resulted in several mutant lines with different localization patterns or signal intensity of GFP-KOR1. One of the identified mutants were disrupted atUDP-glucose:glycoprotein glucosyltransferase(UGGT) locus, which is essential for the protein quality control in the ER. Our finding suggests the mis/unfolded structure of KOR1 triggers the TP targeting.