Semaphorin 1a and semaphorin 1b are required for correct epidermal cell positioning and adhesion during morphogenesis in C. elegans

Development ◽  
2002 ◽  
Vol 129 (9) ◽  
pp. 2065-2078
Author(s):  
Val E. Ginzburg ◽  
Peter J. Roy ◽  
Joseph G. Culotti

The semaphorin family comprises secreted and transmembrane proteins involved in axon guidance and cell migration. We have isolated and characterized deletion mutants of C. elegans semaphorin 1a (Ce-sema-1a or smp-1) and semaphorin 1b (Ce-sema-1b or smp-2) genes. Both mutants exhibit defects in epidermal functions. For example, the R1.a-derived ray precursor cells frequently fail to change anterior/posterior positions completely relative to their sister tail lateral epidermal precursor cell R1.p, causing ray 1 to be formed anterior to its normal position next to ray 2. The ray cells, which normally separate from the lateral tail seam cell (SET) at the end of L4 stage, remains connected to the SET cell even in adult mutant males. The ray 1 defects are partially penetrant in each single Ce-sema-1 mutant at 20°C, but are greatly enhanced in Ce-sema-1 double mutants, suggesting that Ce-Sema-1a and Ce-Sema-1b function in parallel to regulate ray 1 position. Both mutants also have defects in other aspects of epidermal functions, including head and tail epidermal morphogenesis and touch cell axon migration, whereas, smp-1 mutants alone have defects in defecation and brood size. A feature of smp-1 mutants that is shared with mutants of mab-20 (which encodes Sema-2a) is the abnormal perdurance of contacts between epidermal cells.

2016 ◽  
Vol 416 (1) ◽  
pp. 123-135 ◽  
Author(s):  
Stéphanie Grimbert ◽  
Kyria Tietze ◽  
Michalis Barkoulas ◽  
Paul W. Sternberg ◽  
Marie-Anne Félix ◽  
...  

2016 ◽  
Author(s):  
Samantha N. Hartin ◽  
Meagan Kurland ◽  
Brian D. Ackley

AbstractCell adhesion molecules are key to axon guidance during development, for example specific cues can instruct axons to terminate in a specific area, or to continue growth. Syndecans are conserved cell-surface receptors that function in multiple developmental contexts. Caenorhabditis elegans with mutations in the single syndecan gene, sdn-1, exhibited errors in anterior-posterior guidance, with axons that stopped short of, or grew past their stereotypical termination point. Syndecan function was cell non-autonomous for GABAergic axon outgrowth during early development, but was likely cell autonomous to inhibit growth later in development. sdn-1 appeared to regulate the inhibitory activity of the egl-20/Wnt ligand. Removing egl-20 from sdn-1 mutants resulted in fewer animals with prematurely terminating axons. The proteoglycan modifying enzymes hse-5 and hst-2, but not hst-6, had similar effects, suggesting specific heparan sulfate modifications regulated EGL-20 axon-terminating activity. sdn-1 functioned with lin-17/Frizzled, bar-1/β-catenin and the egl-5 Hox-like transcription factor in EGL-20-depedent axon outgrowth. bar-1 was required for egl-5 expression in the most posterior GABAergic neurons. sdn-1 mutations did not eliminate egl-5 expression, but over-expression of egl-5 rescued sdn-1 phenotypes. Our results suggest syndecan is a component of Wnt-signaling events that are necessary for axons to recognize appropriate termination points.


2022 ◽  
Vol 10 (1) ◽  
pp. 3
Author(s):  
Dana K. Tucker ◽  
Chloe S. Adams ◽  
Gauri Prasad ◽  
Brian D. Ackley

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.


Development ◽  
2000 ◽  
Vol 127 (4) ◽  
pp. 755-767 ◽  
Author(s):  
P.J. Roy ◽  
H. Zheng ◽  
C.E. Warren ◽  
J.G. Culotti

The Semaphorins are a family of secreted and transmembrane proteins known to elicit growth cone repulsion and collapse. We made and characterized a putative null mutant of the C. elegans gene semaphorin-2a (Ce-sema-2a). This mutant failed to complement mutants of mab-20 (Baird, S. E., Fitch, D. H., Kassem, I. A. A. and Emmons, S. W. (1991) Development 113, 515–526). In addition to low-frequency axon guidance errors, mab-20 mutants have unexpected defects in epidermal morphogenesis. Errant epidermal cell migrations affect epidermal enclosure of the embryo, body shape and sensory rays of the male tail. These phenotypic traits are explained by the formation of inappropriate contacts between cells of similar type and suggest that Ce-Sema-2a may normally prevent formation or stabilization of ectopic adhesive contacts between these cells.


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