GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE335nnn/GSE335207/suppl/GSE335207_RNAseq_P_aeruginosa.csv.gzftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE335nnn/GSE335207/suppl/GSE335207_RNAseq_A_fumigatus.csv.gzftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE335nnn/GSE335207/primaryOK200Transcriptomics Aspergillus fumigatusPseudomonas aeruginosaExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE335207GEOGSEfalseDeciphering the early events of the transcriptional dialogue between Aspergillus fumigatus and Pseudomonas aeruginosa in a dual-species biofilmThe polymicrobial biofilm formed by Aspergillus fumigatus and Pseudomonas aeruginosa is clinically significant, particularly in the airways of cystic fibrosis patients, yet the initial transcriptional reprogramming underlying this interaction remains poorly characterized. This study employs dual-species RNA sequencing to decipher the early (48-hour) transcriptional dialogue within a co-culture biofilm model. We reveal that P. aeruginosa adopts a profound state of metabolic arrest and nutrient scavenging when confronted with wild-type A. fumigatus, characterized by a paradoxical downregulation of iron acquisition machinery and a global shift towards transport activity and alternative nutrient catabolism. In response, A. fumigatus exhibits metabolic repression coupled with the induction of stress defense and alternative energy pathways. Disruption of the fungal histidine kinase SlnA, a key signaling component, dramatically alters this interkingdom crosstalk. In the presence of the ΔslnA mutant, P. aeruginosa reactivates canonical starvation responses, including siderophore production and chemotaxis, while the mutant fungus fails to mount an appropriate structural and chemical defense, displaying a transcriptional profile of dysregulated metabolism and vulnerability. Furthermore, the interaction bidirectionally modulates the expression of virulence determinants and secondary metabolite gene clusters in both species, a process significantly influenced by the slnA locus. Our findings define the early transcriptional landscape of this critical fungal-bacterial interaction and establish SlnA as a master regulator of fungal adaptation within a competitive polymicrobial niche.2026/06/19GSE335207GSM9808059GSM9808060GSM9808061GSM9808064GSM9808065GSM9808062GSM98080633655334956335207 Aspergillus fumigatusPseudomonas aeruginosa