Comparative physiological and co-expression network analysis reveals potential hub genes and adaptive mechanisms responsive to NaCl stress in peanut (Arachis hypogaea L.).

Abstract

Background: Salt stress has become a major threat to peanut yield and quality, and salt stress is particularly detrimental to seedling growth. Combined analysis of the physiology and transcriptomics of salt-tolerant variety (NH5) and salt-sensitive variety (FH23) under 200 mM NaCl stress was conducted to identify the key factors influencing the differences in salt tolerance and to investigate the potential regulatory mechanisms and hub genes associated with salt tolerance in peanuts.

Results: Malondialdehyde (MDA) content and electrolyte leakage rate were significantly increased under prolonged NaCl stress, with the increase in FH23 being even more pronounced. NH5 maintained intracellular osmotic homeostasis by accumulating free proline and soluble protein content. In addition, NH5 exhibited higher antioxidant enzyme activity. The net photosynthetic rate (Pn) of NH5 and FH23 decreased by 64.24% and 94.49% after 96 h of stress. The intercellular CO₂ concentration (Ci) of NH5 significantly decreased by 7.82%, while that of FH23 increased by 42.74%. This suggests that non-stomatal limiting factors were the primary cause of the decline in photosynthesis observed in FH23. Transcriptome analysis revealed the presence of 12,612 differentially expressed genes (DEGs) in response to salt stress, with FH23 exhibiting a greater number than NH5. The number of upregulated genes was significantly higher than that of downregulated genes at 24 h of salt stress, whereas the number of downregulated genes exceeded that of upregulated genes at 48 h. Subsequently, Weighted Gene Co-expression Network Analysis (WGCNA) was performed in conjunction with physiological data. Twenty-four hub genes of salt response were identified, which encoded delta-1-pyrroline-5-carboxylate synthase, aldehyde dehydrogenase, SNF1-related protein kinase, magnesium transporter, temperature-induced lipocalin-1, and ERF transcription factors.

Conclusion: A regulatory network for potential salt tolerance in peanuts has been constructed. The findings revealed distinct mechanisms of response to salt tolerance and identified candidate genes for further investigation.