Root-knot nematodes (
Meloidogyne
spp.) are devastating plant pathogens that cause substantial economic losses worldwide. This study uses RNA-seq to profile the transcriptomic responses of
M. incognita
to the culture supernatant of
Streptomyces
sp. TR27, a strain previously shown to induce 67.6% calibrated mortality against
M. incognita
second-stage juveniles at 48 h. At 12 h post treatment, 231 differentially expressed genes (DEG) were identified, including 114 up-regulated and 117 down-regulated genes. Down-regulated genes were enriched in the pathways related to lysosome (lysosomal ATPase, acid hydrolase, and membrane protein) and steroid hormone metabolism. Gene set enrichment analysis (GSEA) further revealed the transcriptional suppression of oxidative phosphorylation (Complexes I-V) and ribosomal protein coding genes at 12 h post treatment. These findings suggest that the
Streptomyces
sp. TR27 supernatant is associated with multi-pathway transcriptional perturbations, including lysosomal homeostasis dysregulation, steroid hormone metabolism impairment, and potential inhibition of mitochondrial energy production and protein translation. This transcriptional signature provides candidate cellular targets and a hypothetical framework for developing actinobacteria-derived biocontrol agents, pending functional validation of direct compound-target interactions.
Results provide novel insights into the molecular mechanisms underlying microbial interactions in the tomato rhizosphere and highlight the potential of P. chlororaphis ToZa7 for effective biological control of FORL.
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A temporally ordered, multi-layered defense network in B. napus is revealed, characterized by sequential metabolic reprogramming, immune signaling activation, and structural reinforcement, providing mechanistic insights into L. biglobosa resistance.
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Investigation of the biocontrol mechanisms of Bacillus velezensis L33a against V. dahliae JR2 in tomato suggests that L33a is a promising biocontrol strain for green management of tomato Verticillium wilt.
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