Abstract
The cell-cell adhesion molecule Fasciclin II (Fas2) has long been studied for its evolutionarily-conserved role in axon guidance. It is also expressed in the follicular epithelium, where together with a similar protein, Neuroglian (Nrg), it helps to drive the reintegration of cells born out of the tissue plane. Remarkably, one Fas2 protein null allele, Fas2(G0336), demonstrates a mild reintegration phenotype, whereas work with the classic null allele Fas2(EB112) showed more severe epithelial disorganization. These observations raise the question of which allele (if either) causes a bona fide loss of Fas2 protein function. The problem is not only relevant to reintegration but fundamentally important to understanding what this protein does and how it works: Fas2(EB112) has been used in at least 37 research articles, and Fas2(G0336) in at least three. An obvious solution is that one of the two chromosomes carries a modifier that either suppresses (Fas2(G0336)) or enhances (Fas2(EB112)) phenotypic severity. We find not only the latter to be the case, but identify the enhancing mutation as Nrg(14), also a classic null allele.