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R2R3 S23 MYB转录因子作为泛素蛋白酶体途径的新靶点以及盐胁迫和脱落酸反应调节剂的表征

Characterization of R2R3 S23 MYB Transcription Factors as Novel Targets of the Ubiquitin Proteasome-Pathway and Regulators of Salt Stress and Abscisic Acid Response.

作者信息

Beathard Chase, Mooney Sutton, Al-Saharin Raed, Goyer Aymeric, Hellmann Hanjo

机构信息

School of Biological Sciences, Washington State University, Pullman, WA, United States.

Department of Applied Biology, Tafila Technical University, At-Tafilah, Jordan.

出版信息

Front Plant Sci. 2021 Aug 19;12:629208. doi: 10.3389/fpls.2021.629208. eCollection 2021.

DOI:10.3389/fpls.2021.629208
PMID:34489986
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8417012/
Abstract

Rapid response to environmental changes and abiotic stress to coordinate developmental programs is critical for plants. To accomplish this, plants use the ubiquitin proteasome pathway as a flexible and efficient mechanism to control protein stability and to direct cellular reactions. Here, we show that all three members of the R2R3 S23 MYB transcription factor subfamily, MYB1, MYB25, and MYB109, are degraded by the 26S proteasome, likely facilitated by a CUL3-based E3 ligase that uses MATH-BTB/POZ proteins as substrate adaptors. A detailed description of , , and expression shows their nuclear localization and specific tissue specific expression patterns. It further demonstrates that elevated expression of MYB25 reduces sensitivities toward abscisic acid, osmotic and salt stress in Arabidopsis, while downregulation of all S23 members results in hypersensitivities. Transcriptional profiling in root and shoot of seedlings overexpressing MYB25 shows that the transcription factor widely affects cellular stress pathways related to biotic and abiotic stress control. Overall, the work extends our knowledge on proteins targeted by CUL3-based E3 ligases that use MATH-BTB/POZ proteins as substrate adaptors and provides first information on all members of the MYB S23 subfamily.

摘要

对环境变化和非生物胁迫做出快速反应以协调发育程序对植物至关重要。为实现这一点,植物利用泛素蛋白酶体途径作为一种灵活高效的机制来控制蛋白质稳定性并指导细胞反应。在此,我们表明R2R3 S23 MYB转录因子亚家族的所有三个成员MYB1、MYB25和MYB109都被26S蛋白酶体降解,可能是由一种基于CUL3的E3连接酶促进的,该连接酶使用MATH - BTB/POZ蛋白作为底物衔接子。对MYB1、MYB25和MYB109表达的详细描述显示了它们的核定位和特定的组织特异性表达模式。进一步证明,MYB25的过表达降低了拟南芥对脱落酸、渗透和盐胁迫的敏感性,而所有S23成员的下调则导致超敏反应。对过表达MYB25的幼苗根和茎进行转录谱分析表明,该转录因子广泛影响与生物和非生物胁迫控制相关的细胞应激途径。总体而言,这项工作扩展了我们对以MATH - BTB/POZ蛋白作为底物衔接子的基于CUL3的E3连接酶所靶向的蛋白质的认识,并提供了关于MYB S23亚家族所有成员的首个信息。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c64e/8417012/13d07a3db596/fpls-12-629208-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c64e/8417012/4a24c3ca2d21/fpls-12-629208-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c64e/8417012/843bffcbc215/fpls-12-629208-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c64e/8417012/3f6bca01826d/fpls-12-629208-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c64e/8417012/d246e890b04b/fpls-12-629208-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c64e/8417012/d6c72dee00ce/fpls-12-629208-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c64e/8417012/bbf264c6fde3/fpls-12-629208-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c64e/8417012/0802905a4c14/fpls-12-629208-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c64e/8417012/13d07a3db596/fpls-12-629208-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c64e/8417012/4a24c3ca2d21/fpls-12-629208-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c64e/8417012/843bffcbc215/fpls-12-629208-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c64e/8417012/3f6bca01826d/fpls-12-629208-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c64e/8417012/d246e890b04b/fpls-12-629208-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c64e/8417012/d6c72dee00ce/fpls-12-629208-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c64e/8417012/bbf264c6fde3/fpls-12-629208-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c64e/8417012/0802905a4c14/fpls-12-629208-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c64e/8417012/13d07a3db596/fpls-12-629208-g008.jpg

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