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Vicente, C. S. L.

Publications and source records attributed to Vicente, C. S. L..

2 recordsLinked to original sources

Sister species, shared and divergent responses: early transcriptomic profiling of Bursaphelenchus xylophilus exposed to Esteya spp.

Bursaphelenchus xylophilus (pinewood nematode, PWN) responds transcriptionally to nematophagous fungi, but the earliest events preceding cuticle penetration are poorly characterized, and whether closely related fungal antagonists elicit comparable responses is unknown. Here, we compared PWN transcriptomic responses to Esteya floridanum V14639 (EF) and E. vermicola CCF3117 (EV) at 1 h post-inoculation (hpi), capturing the onset of host-fungus interaction. Despite their phylogenetic proximity, under our exposure conditions the two fungi elicited partly divergent host responses at 1 hpi. EF induced a broad transcriptional response enriched in peptidase activity and lysosomal pathways, accompanied by downregulation of cuticle structural components. In contrast, EV triggered a narrower response, without the proteolytic and lysosomal enrichment observed with EF. Direct comparison of the two treatments revealed no significantly enriched Gene Ontology categories, although pathway analysis identified DNA replication and repair pathways, comprising genes more highly expressed under EF. Enrichment analyses revealed a shared transcriptional signature in both interactions characterized by downregulation of xenobiotic- and central carbon-metabolism pathways, suggesting an early reduction in xenobiotic detoxification capacity rather than induction of detoxification programs. These findings suggest that phylogenetic proximity does not necessarily predict conserved early transcriptional responses, although comparisons of single isolates cannot separate species-level from isolate-level effects.

microbiology↗

A transcription factor-pair work in concert to regulate gene expression across the life cycle of the pinewood nematode, Bursaphelenchus xylophilus

The migratory endoparasitic pinewood nematode (PWN), Bursaphelenchus xylophilus, is the causal agent of pine wilt disease, causing significant economic and ecological losses in conifer forest ecosystems in Europe and Asia. Understanding the molecular mechanisms regulating PWN parasitism-related genes may lead to new sustainable solutions for control. Based on previous PWN transcriptomic datasets from the pre-parasitic and parasitic stages and from the pharyngeal gland cells (GC), an in silico analysis was performed to identify transcription factors (TF) highly expressed in the GC. Seven candidates TF genes were selected, and their spatial expression validated by in situ hybridisation. From those, two GC-expressed TFs, BXY_079 and BXY_022, each encoding zinc finger domains, were successfully knocked down by RNA interference. Transcriptomic data from silenced BXY_079 and BXY_022 TFs, analysed with existing life cycle specific transcriptomic data, showed that both TFs control genes expressed at similar times, by repressing male-related genes while activating genes expressed during the J3 and D3 stages, yet each represents the extreme of the others minor function. In addition to these common roles, BXY_079 also activates parasitism-related genes in the J2 stage. These BXY_079-activated parasitism-related genes predominantly encode proteins with lytic functions, including secreted peptidases and glycoside hydrolases. Consistent with their proposed role in parasitism, these genes are highly expressed during the parasitic juvenile stages and are likely involved in nematode feeding, tissue penetration, and migration within the host. In contrast, BXY_022 also represses the expression of several genes related to the reproduction system, such as major sperm proteins and cytosolic motility proteins, particularly in the adult male stage. Taken together, both dual-functional TFs work together, non-redundantly, to regulate gene expression across the life cycle, while each is additionally specialised to regulate diverse and distinct gene sets: ranging from genes implicated in lytic parasitic functions to sexual dimorphism.

pathology↗