TY - JOUR
T1 - Molecular Networks Underlying Wheat Resistance and Susceptibility to Pyrenophora tritici-repentis
AU - Ferreira, Larissa Carvalho
AU - Santana, Flavio Martins
AU - Mur, Luis A.J.
N1 - Copyright: © 2025 by the authors.
PY - 2025/11/15
Y1 - 2025/11/15
N2 - Pyrenophora tritici-repentis (Ptr), the causal agent of tan spot, is a necrotrophic fungus that represents a significant threat to wheat production worldwide. The development of resistant cultivars is limited by an incomplete understanding of wheat defence responses against Ptr. Here, weighted gene co-expression network analysis (WGCNA) was applied to RNA-seq data from resistant (Robigus) and susceptible (Hereward) wheat lines before and after Ptr infection to identify coordinated host responses. Eight co-expression modules were identified, three of which were linked to either resistance, susceptibility, or Ptr infection. The resistance-associated module was enriched with chloroplast ribosomal machinery genes (e.g., 50S ribosome-binding GTPase, L28, L6), and transcriptional regulators. This suggested that maintaining chloroplast function, coupled with large-scale transcriptional reprogramming, was important for resistance. The susceptibility-associated module indicated the high expression of post-transcriptional modifiers, including SGS3, RBX1, and SENPs. The Ptr-responsive module showed common responses in both genotypes and included several defence-related genes (nucleotide-binding domain leucine-rich repeat R-genes [NLRs], chitinases, beta-1,3-glucanases) and metabolic pathways, such as phenylpropanoid biosynthesis and nitrogen metabolism (phenylpropanoid ammonia lyase [PAL], cytochrome P450s, glutamine synthase, and ammonium transporters). These results define distinct and shared molecular networks that are linked to resistance and susceptibility, providing valuable candidate genes for functional validation that could ultimately be exploited to enhance wheat resilience against necrotrophic fungal pathogens.
AB - Pyrenophora tritici-repentis (Ptr), the causal agent of tan spot, is a necrotrophic fungus that represents a significant threat to wheat production worldwide. The development of resistant cultivars is limited by an incomplete understanding of wheat defence responses against Ptr. Here, weighted gene co-expression network analysis (WGCNA) was applied to RNA-seq data from resistant (Robigus) and susceptible (Hereward) wheat lines before and after Ptr infection to identify coordinated host responses. Eight co-expression modules were identified, three of which were linked to either resistance, susceptibility, or Ptr infection. The resistance-associated module was enriched with chloroplast ribosomal machinery genes (e.g., 50S ribosome-binding GTPase, L28, L6), and transcriptional regulators. This suggested that maintaining chloroplast function, coupled with large-scale transcriptional reprogramming, was important for resistance. The susceptibility-associated module indicated the high expression of post-transcriptional modifiers, including SGS3, RBX1, and SENPs. The Ptr-responsive module showed common responses in both genotypes and included several defence-related genes (nucleotide-binding domain leucine-rich repeat R-genes [NLRs], chitinases, beta-1,3-glucanases) and metabolic pathways, such as phenylpropanoid biosynthesis and nitrogen metabolism (phenylpropanoid ammonia lyase [PAL], cytochrome P450s, glutamine synthase, and ammonium transporters). These results define distinct and shared molecular networks that are linked to resistance and susceptibility, providing valuable candidate genes for functional validation that could ultimately be exploited to enhance wheat resilience against necrotrophic fungal pathogens.
KW - Pyrenophora tritici-repentis
KW - tan spot disease
KW - Triticum aestivum
KW - necrotrophic pathogen
KW - gene-gene network
UR - https://www.scopus.com/pages/publications/105023199571
U2 - 10.3390/microbiolres16110242
DO - 10.3390/microbiolres16110242
M3 - Article
SN - 2036-7481
VL - 16
JO - Microbiology Research
JF - Microbiology Research
IS - 11
M1 - 242
ER -