# Mechanisms of Increase of Winter Wheat Frost Resistance Under Tebuconazole Treatment at Early Stage of Growth: Role of Hormone- and Reactive Oxygen Species-Mediated Signaling Pathways

## TL;DR

This study explores how tebuconazole treatment increases frost resistance in winter wheat seedlings by activating hormone and reactive oxygen species signaling pathways.

## Contribution

The paper identifies ABA-independent pathways as key in tebuconazole-induced frost resistance in wheat seedlings.

## Key findings

- FLD inhibited carotenoid accumulation but did not suppress growth inhibition by tebuconazole.
- FLD had no significant effect on sugar content or frost resistance in cold-hardened seedlings.
- Tebuconazole activates ABA-independent pathways more than ABA-dependent ones in enhancing frost resistance.

## Abstract

1, 2, 4-triazole derivatives, including tebuconazole, have been reported to show positive physiological effects in cereals apart from fungicidal activity and to increase plants’ tolerance against temperature stress. This study investigates the mechanisms of increasing frost resistance of etiolated winter wheat (Triticum aestivum L., “Irkutskaya” variety) seedlings by tebuconazole-based seed dresser “Bunker” (1.5 μL g−1 of seeds) and tebuconazole (30 μg g−1 of seeds). To identify ABA-dependent and ABA-independent pathways of frost resistance, we used fluridone (FLD, 5 mg L−1), an inhibitor of endogenous abscisic acid (ABA) synthesis. FLD effectively inhibited the accumulation of carotenoids in the shoots and prevented the formation of carotenoids caused by the “Bunker” and tebuconazole. In non-hardened seedlings, FLD stimulated coleoptile and first leaf growth, but did not suppress the growth inhibitory effects of “Bunker” and tebuconazole. In shoots of hardened seedlings, FLD reduced the retarding effect of tebuconazole. Regardless of seedling age, temperature, and the protectant treatment, FLD had no effect on the sugar content in the shoots. FLD did not essentially influence frost resistance induced by “Bunker” and tebuconazole in cold-hardened seedlings. Fluridone increased H2O2 content and guaiacol peroxidase activity under control conditions (both with tebuconazole and without tebuconazole) and during cold hardening (in seedlings from seeds treated with tebuconazole). ABA levels in cold-hardened seedlings treated with FLD alone, tebuconazole alone, or a combination of the two were two to three times lower than in untreated hardened seedlings. Changes in indole-3-acetic and salicylic acids in response to FLD and tebuconazole treatment indicate complex interactions with signaling cellular systems. Our results suggest that tebuconazole activates ABA-independent pathways more strongly than ABA-dependent pathways in enhancing frost resistance. The potential mechanisms of tebuconazole action in plant cells are discussed.