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Key message <p><i>SlERF26</i> acts as an essential downstream node in melatonin signaling, forming a novel regulatory module that integrates ethylene and carotenoid metabolism to drive tomato fruit ripening.</p> Abstract <p>Melatonin is an emerging regulator of plant development and stress responses, yet the specific transcriptional mechanisms by which it modulates climacteric fruit ripening remain largely unclear. In this study, we investigated the physiological effects of exogenous melatonin on tomato (<i>Solanum lycopersicum</i> cv. ‘Micro Tom’) fruit ripening and elucidated the underlying molecular regulatory network. Our results showed that exogenous application of melatonin, particularly at 100&#xa0;μmol·L⁻<sup>1</sup>, significantly accelerated ripening progression, characterized by earlier color transition, elevated soluble sugar levels, and enhanced carotenoid accumulation (especially lycopene). This phenotypic change was accompanied by an earlier and stronger increase in ethylene production and respiration rate at the ripening transition stage. Integrated transcriptomic profiling and weighted gene co-expression network analysis (WGCNA) identified SlERF26, a member of the AP2/ERF superfamily, as a key melatonin-responsive transcription factor that is strongly and positively correlated with ethylene and pigment accumulation traits. Functional characterization using virus-induced gene silencing (VIGS) demonstrated that suppression of <i>SlERF26</i> significantly delayed ripening, impaired chlorophyll degradation, and attenuated the expression of key genes involved in carotenoid (<i>SlPSY1</i>, <i>SlPDS</i>) and ethylene (<i>SlACS2</i>, <i>SlACO1</i>) biosynthesis. In addition, SlERF26 silencing caused enzyme-specific and stage-dependent changes in ripening-related enzymes, including reduced PDS and ACO levels at the 40 DAP transition stage, while PSY levels were increased, possibly reflecting a compensatory response. Furthermore, melatonin supplementation failed to fully rescue the ripening defects in SlERF26-silenced fruits, suggesting that <i>SlERF26</i> contributes to melatonin-associated regulation of ethylene biosynthesis and carotenoid accumulation. Collectively, these findings support a working model in which <i>SlERF26</i> contributes to melatonin-associated regulation of ethylene and carotenoid metabolism during tomato fruit ripening.</p>

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SlERF26 contributes to melatonin-associated regulation of ethylene biosynthesis and carotenoid accumulation during tomato fruit ripening

  • 期刊论文

  • 发表日期：

    2026年7月21日

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  • Zhongqi Tang,
  • Qing Yang,
  • Guangzheng Wang,
  • Jianhua Dou,
  • Jihua Yu

摘要

Key message

SlERF26 acts as an essential downstream node in melatonin signaling, forming a novel regulatory module that integrates ethylene and carotenoid metabolism to drive tomato fruit ripening.

Abstract

Melatonin is an emerging regulator of plant development and stress responses, yet the specific transcriptional mechanisms by which it modulates climacteric fruit ripening remain largely unclear. In this study, we investigated the physiological effects of exogenous melatonin on tomato (Solanum lycopersicum cv. ‘Micro Tom’) fruit ripening and elucidated the underlying molecular regulatory network. Our results showed that exogenous application of melatonin, particularly at 100 μmol·L⁻1, significantly accelerated ripening progression, characterized by earlier color transition, elevated soluble sugar levels, and enhanced carotenoid accumulation (especially lycopene). This phenotypic change was accompanied by an earlier and stronger increase in ethylene production and respiration rate at the ripening transition stage. Integrated transcriptomic profiling and weighted gene co-expression network analysis (WGCNA) identified SlERF26, a member of the AP2/ERF superfamily, as a key melatonin-responsive transcription factor that is strongly and positively correlated with ethylene and pigment accumulation traits. Functional characterization using virus-induced gene silencing (VIGS) demonstrated that suppression of SlERF26 significantly delayed ripening, impaired chlorophyll degradation, and attenuated the expression of key genes involved in carotenoid (SlPSY1, SlPDS) and ethylene (SlACS2, SlACO1) biosynthesis. In addition, SlERF26 silencing caused enzyme-specific and stage-dependent changes in ripening-related enzymes, including reduced PDS and ACO levels at the 40 DAP transition stage, while PSY levels were increased, possibly reflecting a compensatory response. Furthermore, melatonin supplementation failed to fully rescue the ripening defects in SlERF26-silenced fruits, suggesting that SlERF26 contributes to melatonin-associated regulation of ethylene biosynthesis and carotenoid accumulation. Collectively, these findings support a working model in which SlERF26 contributes to melatonin-associated regulation of ethylene and carotenoid metabolism during tomato fruit ripening.