is upregulated by fungal infection in a GPA-12 and STA-2-independent manner in the epidermis.

Skin infection with the fungus leads to a transcriptional response in the worm epidermis. This involves an increased expression of a group of antimicrobial peptide (AMP) genes including those in the and clusters. The major pathways leading to the expression of these AMP genes have been well characterized and converge on the STAT transcription factor STA-2. We reported previously that expression in the epidermis of a constitutively active (gain of function, gf) form of the Gα protein GPA-12 (GPA-12gf) recapitulates much of the response to infection. To reveal parallel pathways activated by infection, we focus here on an effector gene that is not induced by GPA-12gf. This gene, , encodes a protein with a fascin domain, associated with actin binding. Its induction upon fungal infection does not require . A transcriptional reporter revealed induction in the epidermis of by infection and wounding. Thus, represents part of a previously unexplored aspect of the innate immune response to infection.