ELO2 Participates in the Regulation of Osmotic Stress Response by Modulating Nitric Oxide Accumulation in Arabidopsis.

The ELO family is involved in synthesizing very-long-chain fatty acids (VLCFAs) and VLCFAs play a crucial role in plant development, protein transport, and disease resistance, but the physiological function of the plant ELO family is largely unknown. Further, while nitric oxide synthase (NOS)-like activity acts in various plant environmental responses by modulating nitric oxide (NO) accumulation, how the NOS-like activity is regulated in such different stress responses remains misty. Here, we report that the yeast mutant Δ is defective in HO-triggered cell apoptosis with decreased NOS-like activity and NO accumulation, while its Arabidopsis homologous gene could complement such defects in Δ. The expression of this gene is enhanced and required in plant osmotic stress response because the T-DNA insertion mutant is more sensitive to the stress than wild-type plants, and expression could rescue the sensitivity phenotype of . In addition, osmotic stress-promoted NOS-like activity and NO accumulation are significantly repressed in , while exogenous application of NO donors can rescue this sensitivity of in terms of germination rate, fresh weight, chlorophyll content, and ion leakage. Furthermore, stress-responsive gene expression, proline accumulation, and catalase activity are also repressed in compared with the wild type under osmotic stress. In conclusion, our study identifies ELO2 as a pivotal factor involved in plant osmotic stress response and reveals its role in regulating NOS-like activity and NO accumulation.