We have investigated the effects of various axon-guidance mutations on the trajectories of the M2 pharyngeal motor neurons which, in wild-type animals, have their cell bodies located in the posterior pharyngeal bulb and send axonal projections through the isthmus and into the metacorpus. To visualize the M2 neurons, we made use of a pRIC-19::GFP construct which we have chromosomally integrated to establish stable transgenic lines. The figure shows the M2 trajectories as seen under UV microscopy, and in cartoon form on the right. The arrowheads in the figure indicate the location of synapses that are revealed as varicosities in the M2 axons where it innervates the m5 muscle cells through which it travels. This study served three purposes: 1) To determine which part of the trajectories of these neurons involves growth cones; 2) To identify genetic backgrounds where abnormal connectivities of the M2 neurons may be correlated with pharyngeal functional defects; and 3) To determine the feasibility of a screen for axon guidance defects in the M2 neurons. We used our GFP reporter to visualize the M2 neurons in various cell-autonomous and cell-non-autonomous axon guidance mutant backgrounds, as well as in pharyngeal abnormal mutant backgrounds. No M2 projection abnormalities were ever observed in the proximal part of the neuronal trajectories, i.e. between the cell body and the metacorpus. Defects were however observed at the distal ends of the M2 axons, within the metacorpus, where abnormal "bead-like" terminations and inappropriate trajectories were observed in both cell autonomous and cell non-autonomous axon guidance mutant backgrounds, including unc-5, unc-6, unc-51, unc-73 and sax-3. Our results show that the trajectories of the M2 axons are very robust in their proximal sections, that is between the cell body and the metacorpus, but quite sensitive to the effects of known axon guidance mutations in their more distal regions. We propose a model whereby the M2 neurons of the pharyngeal primordium form physical connections with neighboring cells, such as the sister cells M3, that are ultimately located within the metacorpus, and that these connections elongate to form the proximal M2 axon trajectories as the priomordium undergoes morphogenesis. In a screen of approximately 2500 mutagenized haploid genomes, we have found 5 mutants with defects in the distal M2 trajectories, and none affecting the proximal trajectory.