Sly‐miR398b Mediates Mature Leaf Flattening by Orchestrating Auxin and H2O2 Signalling in Tomato

Author:

Zhang Xinshan1,Wang Xiujuan1,Deng Fei2,Liu Yuanyuan13,Ru Lei13,Yan Guochao13,Xu Yunmin13,Zhu Zhujun13ORCID,He Yong13ORCID

Affiliation:

1. Discipline of Facility Horticulture, College of Horticulture Science Zhejiang A&F University Hangzhou Zhejiang China

2. Department of Computer Science and Technology, College of Mathematics and Computer Science Zhejiang A&F University Hangzhou Zhejiang China

3. Key Laboratory of Quality and Safety Control for Subtropical Fruit and Vegetable of Ministry of Agriculture and Rural Affairs Hangzhou Zhejiang China

Abstract

ABSTRACTLeaf flattening plays a pivotal role in optimizing light capture and enhancing photosynthesis efficiency. While extensive research has clarified the molecular mechanisms governing the initial stages of leaf flattening, understanding the maintenance of this process in mature leaves remains limited. Our investigation focused on sly‐miR398b in tomatoes and revealed its crucial role in maintaining leaf flattening. In situ hybridization experiments indicated predominant expression of sly‐miR398b in the abaxial side. Disrupting sly‐miR398b using CRISPR/Cas9 relieved its suppression on target gene (Cu/Zn‐SOD, SlCSD1), elevating SlCSD1 levels specifically on the abaxial side. Consequently, this asymmetrical expression of SlCSD1 increased hydrogen peroxide (H2O2) levels in the abaxial side, hindering auxin influx genes while promoting auxin efflux gene expression. This shift reduced auxin response gene expression in the abaxial side of mature leaves compared to the adaxial side, leading to leaf epinasty in sly‐miR398b mutants. Exogenous H2O2 spraying induced leaf epinasty, downregulating SlGH3.5 and upregulating SlPIN3 and SlPIN4. Remarkably, spraying with 1‐naphthalacetic acid (NAA) restored leaf flattening in sly‐miR398b mutants. Our findings offer novel insights into mature leaf flattening maintenance via sly‐miR398b's regulation of auxin and H2O2 signalling pathways.

Funder

National Natural Science Foundation of China

Publisher

Wiley

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