Abstract
Neurons form elaborate networks by guiding axons and dendrites to appropriate destinations. Neurites require information about the relative body axes during the initial projection from the cell body, and failure to receive or interpret those cues correctly can result in outgrowth errors. We identified a mutation in the Ig superfamily member syg-2 in a screen for animals with anterior/posterior (A/P) axon guidance defects. We found that syg-2 and its cognate Ig family member syg-1 appear to function in a linear genetic pathway to control the outgrowth of GABAergic axons. We determined that this pathway works in parallel to Wnt signaling. Specifically, mutations in syg-2 or syg-1 selectively affected the embryonically derived Dorsal D-type (DD) GABAergic neurons. We found no evidence that these mutations affected the Ventral D-type neurons (VD) that form later, during the first larval stage. In addition, mutations in syg-1 or syg-2 could result in the DD neurons forming multiple processes, becoming bipolar, rather than the expected pseudounipolar morphology. Given SYG-2′s essential function in synaptogenesis of the hermaphrodite-specific neurons (HSNs), we also examined DD neuron synapses in syg-2 mutants. We found syg-2 mutants had a decreased number of synapses formed, but synaptic morphology was largely normal. These results provide further evidence that the GABAergic motorneurons use multiple guidance pathways during development.
Highlights
Nervous system development is a complex process that is, to a degree, orchestrated by secreted and cell surface-associated molecules that work together to achieve the finished product
In contrast to previous reports of syg-1 and syg-2 dramatically affecting hermaphrodite-specific neurons (HSNs) synapse formation, we found a mild effect of syg-2 loss-of-function mutations on synaptogenesis in GABAergic neurons
In syg-2 or syg-1 mutants, the penetrance of posteriorly directed neurite (Pdn) was equivalent in L1s or adults (Figure 4D–L, Table 2), suggesting that the Dorsal D-type (DD) neurons
Summary
Nervous system development is a complex process that is, to a degree, orchestrated by secreted and cell surface-associated molecules that work together to achieve the finished product. In fmi-1 mutants, Pdns form exclusively in the Ventral D-type (VD), but not the Dorsal D-type (DD), GABAergic motorneurons [1] In this context, FMI-1 functions cell non-autonomously to regulate GABAergic neuron development [1]. We discovered that Pdn defects in fmi-1 mutants are synergistically enhanced by mutations in Wnt signaling pathway genes, suggesting that they function in parallel genetic pathways. Syg-2 is an evolutionarily conserved member of the Ig superfamily (IgSF) of cell adhesion molecules This group of molecules is characterized by the presence of immunoglobulin (Ig)like motifs, often in the extracellular domain, where they exhibit homophilic or heterophilic interactions, typically, but not exclusively, with other IgSF proteins. Regulating axon outgrowth in parallel to Wnt signaling to prevent the formation of ectopic secondary neurites in DD neurons. Our results suggest that these proteins likely function differently in these neuron types
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