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Active protein ubiquitination regulates xylem vessel functionality
The Plant Cell ( IF 10.0 ) Pub Date : 2024-08-02 , DOI: 10.1093/plcell/koae221
Pawittra Phookaew 1 , Ya Ma 2 , Takaomi Suzuki 1 , Sara Christina Stolze 3 , Anne Harzen 3 , Ryosuke Sano 1 , Hirofumi Nakagami 3 , Taku Demura 1, 4 , Misato Ohtani 1, 2, 4
Affiliation  

Xylem vessels function in the long-distance conduction of water in land plants. The NAC transcription factor VASCULAR-RELATED NAC-DOMAIN7 (VND7) is a master regulator of xylem vessel cell differentiation in Arabidopsis (Arabidopsis thaliana). We previously isolated suppressor of ectopic xylem vessel cell differentiation induced by VND7 (seiv) mutants. Here, we report that the responsible genes for seiv3, seiv4, seiv6, and seiv9 are protein ubiquitination-related genes encoding PLANT U-BOX46 (PUB46), an uncharacterized F-BOX protein (FBX), PUB36, and UBIQUITIN-SPECIFIC PROTEASE1 (UBP1), respectively. We also found decreased expression of genes downstream of VND7 and abnormal xylem transport activity in the seiv mutants. Upon VND7 induction, ubiquitination levels from 492 and 180 protein groups were upregulated and downregulated, respectively. VND7 induction resulted in the ubiquitination of proteins for cell wall biosynthesis and protein transport, whereas such active protein ubiquitination did not occur in the seiv mutants. We detected the ubiquitination of three lysine residues in VND7: K94, K105, and K260. Substituting K94 with arginine significantly decreased the transactivation activity of VND7, suggesting that the ubiquitination of K94 is crucial for regulating VND7 activity. Our findings highlight the crucial roles of target protein ubiquitination in regulating xylem vessel activity.

中文翻译:


活性蛋白泛素化调节木质部血管功能



木质部血管在陆地植物中起长距离传导水的作用。NAC 转录因子 VASCULAR-RELATED NAC-DOMAIN7 (VND7) 是拟南芥 (Arabidopsis thaliana) 中木质部血管细胞分化的主要调节因子。我们之前分离了 VND7 (seiv) 突变体诱导的异位木质部血管细胞分化的抑制因子。在这里,我们报道了 seiv3、seiv4、seiv6 和 seiv9 的负责基因是编码植物 U-BOX46 (PUB46)、未表征的 F-BOX 蛋白 (FBX)、PUB36 和泛素特异性PROTEASE1 (UBP1) 的蛋白质泛素化相关基因。我们还发现 VND7 下游基因的表达降低,以及 seiv 突变体中木质部转运活性异常。VND7 诱导后,492 和 180 个蛋白组的泛素化水平分别上调和下调。VND7 诱导导致蛋白质泛素化用于细胞壁生物合成和蛋白质运输,而这种活性蛋白质泛素化在 seiv 突变体中未发生。我们在 VND7 中检测到三个赖氨酸残基的泛素化:K94、K105 和 K260。用精氨酸取代 K94 显著降低了 VND7 的反式激活活性,表明 K94 的泛素化对于调节 VND7 活性至关重要。我们的研究结果强调了靶蛋白泛素化在调节木质部血管活性中的关键作用。
更新日期:2024-08-02
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