ArticleJournal of experimental botany2026
Sulfite dynamics affect drought tolerance and water status in Arabidopsis and tomato.
Article in Journal of experimental botany, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Previously, we showed that altered sulfite homeostasis led to higher water loss in sulfite oxidase (SO) RNA interference (Ri) plants than in Arabidopsis wild type (WT) after sulfite infiltration into rosette leaves. In contrast, SO overexpression (OE) and adenosine-5'-phosphosulfate reductase 2 (apr2) knockout (KO) resulted in lower water loss than in WT. Accordingly, sulfite homeostasis and drought tolerance under prolonged drought in Arabidopsis and tomato (Rheinlands Ruhm) were investigated. SO Ri mutants displayed the most severe wilting and water loss, accompanied by sulfite accumulation due to reduced SO expression. In contrast, SO OE, apr2 KO, apr2 KO/SO OE, and gene-edited lines, including sulfite reductase (SiR) OEC2+SO OEC2 and SiR OEC4/SO OE, maintained higher relative water content by enhancing sulfite oxidation and reduction. Elevated sulfite in SO Ri mutants acted as an antagonist to abscisic acid (ABA), as despite accumulating higher ABA than all other genotypes, SO Ri plants displayed the lowest relative water content, consistent with sulfite suppressing ABA signal transduction through impaired by Pyrobactin resistance 1-like 5 (PYL5) and enhanced ABA negative feedback by Highly ABA-induced PP2C gene 2 (HAI2). SO and SiR overexpression also increased hydrogen sulfide and cysteine levels, contributing to drought resilience. Tomato lines also reflected these patterns in SO OE, SiR OE, and SiR OE/SO OE, showing reduced sulfite and improved relative water content compared with WT. Overall, coordinated regulation of SO, SiR, and APR2 maintains sulfite homeostasis, mitigating drought-induced damage and enhancing water retention across species by directly limiting sulfite accumulation and relieving sulfite-driven antagonism of ABA signal transduction.
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