Ascidian metamorphosis transforms a free-swimming larval chordate ascidian into a sessile adult through a distinct series of metamorphic events. Initially, larvae must become competent to respond to settlement cues. Settlement is then marked by dramatic body plan remodeling and may be accompanied by attachment to the substrate. Subtractive hybridization has revealed that many innate immunity transcripts are upregulated during metamorphosis in the ascidian Boltenia villosa. Several of these genes have well-known roles in the mannose-binding lectin (MBL)-complement pathway of innate immunity, including MBL and MBL-activated serine protease (MASP). MBL recognizes and binds to bacterial pathogens, activates MASP, and triggers the complement cascade. In B. villosa, larvae upregulate BvMASP at the time of competency to initiate settlement. We show that several bacterial strains can induce settlement and that the timing of BvMASP expression in the papillae-associated tissue (PAT) cells is tightly correlated with larval competency. We further demonstrate that serine protease inhibitors used to block the complement response also block metamorphosis, allowing tail resorption, but preventing further morphological changes. Based on these experiments, we propose that the MBL-complement pathway may be important for competency, bacterial substrate detection and body plan remodeling during metamorphosis.