ABSTRACT 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) and trans-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 at UDP-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.

中文翻译：

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缺乏内质网质量控制 (ERQC) 促进液泡膜 (TP) 靶向 KORRIGAN 1 (KOR1)

摘要 KORRIGAN 1 (KOR1) 的细胞动力学与纤维素生物合成和植物渗透胁迫耐受性密切相关。KOR1 在质膜 (PM) 和反式高尔基网络 (TGN) 之间的循环由细胞运输和质量控制机制识别的序列基序和蛋白质结构维持。KOR1 中的几个突变以及宿主遗传背景中的突变促进了 KOR1 的错误定位并诱导了 KOR1 在液泡膜 (TP) 中的积累。然而，关于 KOR1 的保留和分类如何在 PM-TG​​N 循环中受到调节知之甚少。对 GFP-KOR1 错误定位表型的正向遗传筛选导致了几个具有不同定位模式或 GFP-KOR1 信号强度的突变系。鉴定的突变体之一在 UDP-葡萄糖处被破坏：糖蛋白葡萄糖基转移酶 (UGGT) 基因座，这对于 ER 中的蛋白质质量控​​制至关重要。我们的发现表明 KOR1 的错误/未折叠结构触发了 TP 靶向。