Abstract

High salinity-induced Na+ toxicity and osmotic stress in the rhizosphere environment seriously jeopardize and limit plant growth and development and crop productivity. Trichomes are epidermal outgrowths that contribute to plant defense responses against abiotic stresses. Here, we showed that the expression of NtCycB2 gene in wild flue-cured K326, a B-type cyclin involved in the negative regulation of trichomes density, was induced by NaCl stress. Enhanced high salinity-resistance was observed in NtCycB2 knockout (ko) lines with high-density glandular trichomes, whereas it was the opposite in an NtCycB2 overexpression (OE) line with low-density glandular trichomes. NtCycB2 gene knockout reduced cell death, O2− accumulation, and water loss ratio after different concentrations of NaCl treatments, caused by upregulation of superoxide dismutase (SOD), peroxidase (POD), proline (Pro), higher expression levels of ABA-meditated salinity stress responsive genes, and downregulation of malondialdehyde (MDA). Additionally, NtCycB2 gene knockout had a crucial capacity to reduce Na+ content and improve the K+/Na+ ratio for maintaining ion homeostasis with more intact glandular trichomes under NaCl stress. Increased expression levels of Na+ and K+ uptake or transport genes were positively correlated with NaCl resistance. Together, these data suggested that NtCycB2 acted as a negative regulator and conferred high salinity-resistance. High-density glandular trichomes be an important botanical trait to improve plant resistance.

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