A heat-shock 20 protein isolated from watermelon (ClHSP22.8) negatively regulates the response of Arabidopsis to salt stress via multiple signaling pathways

Heat-shock protein 20s (HSP20) were initially shown to play a role during heat shock stress; however, recent data indicated that HSP20 proteins are also involved in abiotic stress in plants. Watermelon is known to be vulnerable to various stressors; however, HSP20 proteins have yet to be investigated and characterized in the watermelon. In a previous study, we identified a negative regulator of salt stress response from watermelon: ClHSP22.8, a member of the HSP20 family. Quantitative real-time PCR (qRT-PCR) and promoter::beta-glucuronidase (GUS) analysis revealed that ClHSP22.8 was expressed widely in a range of different tissues from the watermelon, but particularly in the roots of 7-day-old seedlings and flowers. Furthermore, qRT-PCR and GUS staining showed that the expression of ClHSP22.8 was significantly repressed by exogenous abscisic acid (ABA) and salt stress. The over-expression of ClHSP22.8 in Arabidopsis lines resulted in hypersensitivity to ABA and reduced tolerance to salt stress. Furthermore, the expression patterns of key regulators associated with ABA-dependent and independent pathways, and other stress-responsive signaling pathways, were also repressed in transgenic lines that over-expressed ClHSP22.8. These results indicated that ClHSP22.8 is a negative regulator in plant response to salt stress and occurs via ABA-dependent and independent, and other stress-responsive signaling pathways.

Automated summary

The study identified ClHSP22.8 as a negative regulator in response to salt stress in watermelon, influencing plant sensitivity to ABA and tolerance to salt stress. The over-expression of ClHSP22.8 in transgenic Arabidopsis lines led to repression of key regulators associated with ABA-dependent and independent pathways, as well as other stress-responsive signaling pathways. ClHSP22.8 is suggested to play a critical role in mediating plant responses to salt stress through ABA-dependent and independent pathways.