Fecha de publicación: 20/01/2025 Fuente: PubMed "nature biotechnology" 3 Biotech. 2025 Feb;15(2):44. doi: 10.1007/s13205-025-04211-x. Epub 2025 Jan 16.ABSTRACTSclerotium rolfsii is the causal agent of stem rot of many crops, a highly destructive disease of groundnut (Arachis hypogaea L.). Based on evidence that many groundnut genotypes have an inherent ability to tolerate the pathogenicity of Sclerotium species, twenty-two genotypes of groundnut were screened against Sclerotium rolfsii infection in sick plot field experiment; four genotypes, namely CS19, GG16, GG20 and TG37A, were selected as being the most tolerant, moderately tolerant, susceptible and highly susceptible to stem rot, respectively. Stem tissues (1cm from the collar region) from infected and healthy plants of four selected genotypes differing in Sclerotium rolfsii susceptibility were examined using a scanning electron microscope (SEM). Differential formation and deposition of tyloses, calcium-oxalate, and fibrillar networks were observed in xylem tissue elements in tolerant and susceptible genotypes in infected plants. To elucidate the mechanisms underlying the defense responses and tolerance to stem rot in groundnut plants, the patterns of pathogenesis-related proteins (PR) and polygalacturonase inhibiting protein (PGIP) gene expression in the selected genotypes were studied using qRT-PCR. Genes encoding PR-proteins are the most important inducible defense-related antifungal proteins and the genes encoding PGIP that inhibit the pectin-depolymerizing were highly expressed in the tolerant genotype as compared to the susceptible genotype, suggesting that PR and PGIP are important components for Sclerotium rolfsii tolerance in groundnut. Results of cis-regulatory elements analysis of PGIP promoter regions showed enrichment of ERF, MYB and bHLH transcription factors binding sites that are known to be preferentially and co-ordinately expressed during various stresses.SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s13205-025-04211-x.PMID:39829642 | PMC:PMC11739059 | DOI:10.1007/s13205-025-04211-x