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Hydrogen sulfide-mediated persulfidation of ERF106 controls pear fruit aroma biosynthesis via disrupting the ERF106-MYB21-FAD8 complex.

Created on 18 Sep 2026

Authors

Zhuoyan Xu, Kangdi Hu, Longfei Yan, Shuwei Wei, Weisheng Zhao, Huihui Song, Gaifang Yao, Hua Zhang

Published in

The Plant journal : for cell and molecular biology. Volume 127. Issue 6. Pages e71129.

Abstract

Hydrogen sulfide (H2S) and its mediated protein persulfidation regulate fruit ripening. Fruit aroma, a key quality trait formed during ripening, largely determines consumer preferences. However, the mechanism by which H2S modulates aroma biosynthesis in pear remains unclear. This study reveals that H2S inhibited aroma biosynthesis in 'Nanguo' pear and downregulated the fatty acid desaturase gene PuFAD8. Transient overexpression and silencing assays confirmed that PuFAD8 was required for linoleic acid synthesis, a key aroma precursor. Heterologous overexpression of PuFAD8 in tomato and its knockout in tomato further validated that PuFAD8 promoted fruit aroma formation, while H2S suppressed this function. Transcriptome analysis identified transcription factors PuMYB21 and PuERF106 co-expressed with PuFAD8. Dual-luciferase and yeast one-hybrid assays revealed that PuMYB21 bound and activated the PuFAD8 promoter. Moreover, Y2H, luciferase complementation, pull-down, and transient expression assays demonstrated that PuERF106 interacted with PuMYB21, synergistically enhancing aroma biosynthesis. Persulfidation at Cys162 of PuERF106 attenuated its interaction with PuMYB21, thereby inhibiting aromatic compound synthesis in pear fruit. Subsequently, the biological function of the PuERF106-PuMYB21-PuFAD8 molecular module was validated using stable transgenic pear callus lines and a panel of heterologous and endogenous transgenic tomato lines. This study reveals a novel regulatory mechanism where H2S-mediated persulfidation suppresses pear aroma biosynthesis, providing a theoretical basis for genetic improvement of high-quality pear.

PMID:
42758115
Bibliographic data and abstract were imported from PubMed on 18 Sep 2026.

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