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Understanding the molecular switch that limits tomato drought tolerance

Plants rely on finely tuned hormonal signaling to survive drought and salinity, yet the molecular mechanisms that integrate competing stress signals remain incompletely understood. This study identifies a key transcription factor, SlERF.D2, as a negative regulator of osmotic stress adaptation in tomato. Through coordinated physiological, genetic, and molecular analyses, the research reveals that SlERF.D2 weakens drought and salt tolerance by impairing stomatal closure and disrupting redox homeostasis. By linking ethylene signaling to suppression of abscisic acid (ABA) responses, SlERF.D2 emerges as a critical node that balances water conservation, reactive oxygen species control, and stress sensitivity, highlighting an unexpected mechanism that limits plant resilience under harsh environmental conditions.

Drought and soil salinity impose osmotic stress that severely restricts crop productivity worldwide. To cope with these challenges, plants deploy complex hormonal networks that regulate water loss, antioxidant defenses, and cellular homeostasis. Abscisic acid (ABA) is a central driver of stress-induced stomatal closure, while ethylene often counteracts ABA-mediated responses. Although antagonism between these hormones has been observed, the molecular links that integrate ethylene and ABA signaling remain poorly resolved. In parallel, reactive oxygen species act as both signaling molecules and damaging agents, requiring tight regulatory control. Based on these challenges, there is a pressing need to investigate the molecular mechanisms that coordinate hormone crosstalk and redox regulation during osmotic stress adaptation.

A research team from Fudan University reports (DOI: 10.1093/hr/uhaf267) on 1 January 2026 in Horticulture Research that a previously uncharacterized transcription factor, SlERF.D2, plays a pivotal role in shaping tomato responses to drought and salinity. By combining CRISPR-based gene editing, transcriptomics, and physiological assays, the researchers demonstrate that SlERF.D2 acts as a molecular brake on stress tolerance. Their findings reveal how ethylene signaling suppresses ABA-driven stomatal closure through a defined transcriptional cascade, offering new insight into hormonal coordination during plant stress adaptation.

The study shows that SlERF.D2 expression is rapidly induced by drought, salt stress, and treatments with both ethylene and ABA. Surprisingly, genetic analyses revealed that this induction does not enhance stress resistance. Instead, tomato plants overexpressing SlERF.D2 exhibited accelerated wilting, reduced water retention, impaired photosynthetic efficiency, and excessive accumulation of reactive oxygen species under drought and salt stress. In contrast, SlERF.D2 knockout plants displayed enhanced tolerance, with improved stomatal closure, higher anthocyanin accumulation, and lower oxidative damage.

Mechanistically, the researchers uncovered a transcriptional cascade in which ethylene-activated EIN3/EIL transcription factors directly stimulate SlERF.D2 expression. SlERF.D2 then binds to the promoter of SlPP2C1, a negative regulator of ABA signaling, activating its transcription. Elevated SlPP2C1 suppresses ABA-induced stomatal closure, accelerating water loss during osmotic stress. At the same time, SlERF.D2 represses genes involved in anthocyanin biosynthesis, weakening antioxidant capacity and disrupting redox homeostasis. Together, these effects position SlERF.D2 as a central integrator of hormone antagonism and oxidative balance that ultimately limits stress adaptation in tomato.

"Our findings reveal that not all stress-induced genes enhance tolerance—some actively restrain it," said the study's senior author. "SlERF.D2 functions as a molecular switch that integrates ethylene and ABA signaling, but the outcome is reduced drought resistance rather than protection. This work highlights the importance of understanding negative regulators in stress pathways, as removing or fine-tuning these brakes may be just as important as activating positive defenses when breeding crops for extreme environments."

By identifying SlERF.D2 as a negative regulator of osmotic stress tolerance, this research provides a promising target for crop improvement strategies. Selective suppression of SlERF.D2 or its downstream signaling components could enhance water-use efficiency, strengthen antioxidant defenses, and improve resilience to drought and salinity without compromising growth. Beyond tomato, the ethylene–ABA antagonistic module uncovered here may represent a conserved mechanism across crops. Understanding and manipulating such hormonal cross-talk could support the development of climate-resilient varieties, contributing to sustainable agriculture in regions increasingly threatened by water scarcity and soil salinization.

Source: Eureka Alert

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