Abscisic acid homeostasis is mediated by feedback regulation of MdMYB88 and MdMYB124

Abstract The phytohormone abscisic acid (ABA) is involved in various plant processes. In response to drought stress, plants quickly accumulate ABA, but the regulatory mechanism of ABA accumulation is largely unknown, especially in woody plants. In this study, we report that MdMYB88 and MdMYB124 are...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Journal of experimental botany 2021-02, Vol.72 (2), p.592-607
Hauptverfasser: Xie, Yinpeng, Bao, Chana, Chen, Pengxiang, Cao, Fuguo, Liu, Xiaofang, Geng, Dali, Li, Zhongxing, Li, Xuewei, Hou, Nan, Zhi, Fang, Niu, Chundong, Zhou, Shuangxi, Zhan, Xiangqiang, Ma, Fengwang, Guan, Qingmei
Format: Artikel
Sprache:eng
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Abstract The phytohormone abscisic acid (ABA) is involved in various plant processes. In response to drought stress, plants quickly accumulate ABA, but the regulatory mechanism of ABA accumulation is largely unknown, especially in woody plants. In this study, we report that MdMYB88 and MdMYB124 are myeloblastosis (MYB) transcription factors critical for ABA accumulation in apple trees (Malus x domestica) following drought, and this regulation is negatively controlled by ABA. MdMYB88 and MdMYB124 positively regulate leaf water transpiration, photosynthetic capacity, and stress endurance in apple trees under drought conditions. MdMYB88 and MdMYB124 regulate the expression of biosynthetic and catabolic genes of ABA, as well as drought- and ABA- responsive genes. MdMYB88 associates with promoter regions of the ABA biosynthetic gene 9-cis-epoxycarotenoid dioxygenase 3 (NCED3). Finally, expression of MdMYB88 and MdMYB124 is repressed by ABA. Our results identify a feedback regulation of MdMYB88 and MdMYB124 in modulating ABA homeostasis in apple trees. MdMYB88 and MdMYB124 mediate ABA homeostasis in apple trees following drought by regulating the expression of ABA metabolism-related genes in a negative feedback response.
ISSN:0022-0957
1460-2431
DOI:10.1093/jxb/eraa449