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Disrupting two Arabidopsis thaliana xylosyltransferase genes results in plants deficient in thermomorphogenesis.

Created on 02 Oct 2026

Authors

Yue Liu, Jie Wang, MeLongying Wangzha, Baoguo Wu, Qianwen Zhang, Chunli Zhang, Yujie Wu, Yizhuo Mu, Keyan Zhang, Junhong Zhang, Zhaojun Liu, Sridevi Sureshkumar, Yubao Lv, Yumeng Yang, Li Lin, Sureshkumar Balasubramanian, Chaowen Xiao, Baocai Zhang, Ruohe Yin

Published in

The New phytologist. Oct 01, 2026. Epub Oct 01, 2026.

Abstract

Several cell-wall-modifying enzymes have been implicated in hypocotyl elongation; however, whether cell wall biosynthesis enzymes contribute to this process, particularly under warm temperature, remains largely unknown. In Arabidopsis, xyloglucan is a major component of the primary cell wall. Xyloglucan xylosyltransferase 1 (XXT1) and XXT2 are the major enzymes required for xyloglucan biosynthesis. Here, we investigated the roles of XXT1/2 in hypocotyl elongation with a focus under warm temperature using genetic, molecular, and transcriptomic approaches. We show that XXT1/2 are required for warm-temperature-promoted hypocotyl elongation and that the elongation phenotypes of PHYTOCHROME-INTERACTING FACTOR 4 (PIF4) overexpression, Phytochrome B (phyB), and ELONGATED HYPOCOTYL 5 (hy5) depend partly on XXT1/2. PIF4 directly binds to and activates the promoters of XXT1 and XXT2, whereas HY5 binds to the same promoter regions and represses their expression. Importantly, the warm-temperature-induced increase in xyloglucan content is antagonistically regulated by PIF4 and HY5. Transcriptomic analyses identified warm-responsive genes whose induction depends on XXT1/2, including expansins (EXPs) and xyloglucan endotransglucosylase/hydrolases (XTHs). Mutants of some EXPs and XTHs showed compromised warm-induced hypocotyl elongation. Together, our findings identify XXT1/2 as new components of the phyB-PIF4-HY5 growth network, linking environmental signaling to the cell wall biosynthetic machinery required for hypocotyl elongation.

PMID:
42823822
Bibliographic data and abstract were imported from PubMed on 02 Oct 2026.

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