Homologs and Transcriptional Isoforms of Dorsal Are Involved in the Response of Apis cerana to Ascosphaera apis Infection.

Chalkbrood disease caused by Ascosphaera apis threatens honey bee brood, yet the transcriptional mechanisms that coordinate antifungal immune responses in Apis cerana remain unclear. Here, RNA interference (RNAi) was used to examine two Dorsal homologs and selected dorsal1 transcript isoforms during larval infection. A. apis inoculation increased dorsal1, dorsal2, and five antimicrobial peptide (AMP) transcripts in larval midguts, consistent with an infection-associated humoral response. Gene-level RNAi produced selective transcript responses: dorsal1 knockdown was accompanied by reduced apidaecin and defensin1 expression, whereas dorsal2 knockdown was accompanied principally by reduced defensin1 expression. abaecin, defensin2, and hymenoptaecin transcripts were not significantly altered after dorsal knockdown under the tested conditions. Isoform-targeted RNAi of RNA9886, RNA9888, and RNA9890 was likewise associated with distinct AMP transcript responses, with RNA9888 and RNA9890 more closely associated with defensin1. These transcript-level data support selective and partially overlapping Dorsal-associated regulation during the A. cerana larval response to A. apis, while direct differences in Dorsal protein abundance or activity remain to be established.