Integrated Metabolomic and Transcriptomic Analyses Reveal the Potential Molecular Mechanism Underlying Callus Browning in Paeonia ostii
文献类型： 外文期刊
第一作者： Wen, Xiaohui
作者： Wen, Xiaohui;Xu, Wenting;Zhang, Lili;Shi, Xiaohua;Zhou, Jianghua;Liu, Huichun;Zhu, Kaiyuan
作者机构：
关键词：
callus browning;
期刊名称：PLANTS-BASEL （ 影响因子：4.1； 五年影响因子：4.5 ）
ISSN： 2223-7747
年卷期： 2025 年 14 卷 4 期
页码：
收录情况： SCI
摘要： Callus browning is a significant problem that hinders plant tissue regeneration in Paeonia ostii "Fengdan" by causing cell death and inhibiting growth. However, the molecular mechanism underlying callus browning in P. ostii remains unclear. In this study, we investigated the metabolites and potential regulatory genes involved in callus browning of P. ostii using metabolomic and transcriptomic analyses. We found a significant accumulation of phenolic compounds in the browned callus, represented by flavonoid compounds. Notably, the accumulations of luteotin and disomentin were higher in browning calli compared to non-browning calli. Transcriptomic analysis identified that candidate genes associated with flavonoid biosynthesis, including flavonoid 3-hydroxylase (PoF3H) and flavone synthase II (PoFNSII), were highly expressed in the browned callus of P. ostii "Fengdan". Weighted gene co-expression network analysis (WGCNA) further highlighted that polyphenol oxidase (PoPPO) which encoded polyphenol oxidase, together with flavonoid biosynthesis-related genes such as flavanone 3-hydroxylase (PoF3H) and flavonone Synthase II (PoFNSII), as well as cellular totipotency-related genes wuschel-related homeobox 4 (PoWOX4), were involved in callus browning. Based on these findings, we proposed the molecular mechanism by which flavonoid accumulation, polyphenol oxidation, and cellular totipotency pathways contribute to callus browning in P. ostii. Our study provides new insights into the molecular mechanism underlying callus browning and offers the foundations to facilitate the establishment of an efficient plant tissue regeneration system in P. ostii.
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