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Characterization of Arabidopsis eskimo1 reveals a metabolic link between xylan O-acetylation and aliphatic glucosinolate metabolism

Glucuronoxylan is present mainly in the dicot of the secondary cell walls, often O-acetylated, which stabilizes cell structure by maintaining interaction with cellulose and other cell wall components. Some members of the Golgi localized Trichome Birefringence-Like (TBL) family function as xylan O-ac...

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Bibliographic Details
Published in:Physiologia plantarum 2024-11, Vol.176 (6), p.e14618
Main Authors: Singh, Deepika, Zhao, Haohao, Gupta, Sonu Kumar, Kumar, Yashwant, Kim, Jeongim, Pawar, Prashant Anupama-Mohan
Format: Article
Language:English
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Summary:Glucuronoxylan is present mainly in the dicot of the secondary cell walls, often O-acetylated, which stabilizes cell structure by maintaining interaction with cellulose and other cell wall components. Some members of the Golgi localized Trichome Birefringence-Like (TBL) family function as xylan O-acetyl transferase (XOAT). The primary XOAT in the stem of Arabidopsis is ESKIMO1/TBL29, and its disruption results in decreased xylan acetylation, stunted plant growth, and collapsed xylem vessels. To elucidate the effect on metabolic reprogramming and identify the underlying cause of the stunted growth in eskimo1, we performed transcriptomic, targeted, and untargeted metabolome analysis, mainly in the inflorescence stem tissue. RNA sequencing analysis revealed that the genes involved in the biosynthesis, regulation, and transport of aliphatic glucosinolates (GSLs) were upregulated, whereas those responsible for indolic GSL metabolism were unaffected in the eskimo1 inflorescence stem. Consistently, aliphatic GSLs, such as 4-methylsulfinylbutyl (4MSOB), were increased in stem tissues and seeds. This shift in the profile of aliphatic GSLs in eskimo1 was further supported by the quantification of the soluble acetate, decrease in accumulation of GSL precursor, i.e., methionine, and increase in the level of jasmonic acid.
ISSN:0031-9317
1399-3054
1399-3054
DOI:10.1111/ppl.14618