5
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: not found
      • Article: not found

      Semaphorin-1 and Netrin Signal in Parallel and Permissively to Position the Male Ray 1 Sensillum inCaenorhabditis elegans

      , , ,

      Genetics

      Genetics Society of America

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Netrin and semaphorin axon guidance cues have been found to function in the genesis of several mammalian organs; however, little is known about the underlying molecular mechanisms involved. A genetic approach could help to reveal the underpinnings of these mechanisms. The most anterior ray sensillum (ray 1) in the Caenorhabditis elegans male tail is frequently displaced anterior to its normal position in smp-1/semaphorin-1a and plexin-1/plx-1 mutants. Here we report that UNC-6/netrin and its UNC-40/DCC receptor signal in parallel to SMP-1/semaphorin-1a and its PLX-1/plexin-1 receptor to prevent the anterior displacement of ray 1 and that UNC-6 plus SMP-1 signaling can account entirely for this function. We also report that mab-20/semaphorin-2a mutations, which prevent the separation of neighboring rays and cause ray fusions, suppress the anterior displacements of ray 1 caused by deficiencies in SMP-1 and UNC-6 signaling and this is independent of the ray fusion phenotype, whereas overexpression of UNC-40 and PLX-1 cause ray fusions. This suggests that for ray 1 positioning, a balance is struck between a tendency of SMP-1 and UNC-6 signaling to prevent ray 1 from moving away from ray 2 and a tendency of MAB-20/semaphorin-2a signaling to separate all rays from each other. Additional evidence suggests this balance involves the relative adhesion of the ray 1 structural cell to neighboring SET and hyp 7 hypodermal cells. This finding raises the possibility that changes in ray 1 positioning depend on passive movements caused by attachment to the elongating SET cell in opposition to the morphologically more stable hyp 7 cell. Several lines of evidence indicate that SMP-1 and UNC-6 function permissively in the context of ray 1 positioning.

          Related collections

          Most cited references 52

          • Record: found
          • Abstract: found
          • Article: not found

          C. elegans: des neurones et des gènes

          The human brain contains 100 billion neurons and probably one thousand times more synapses. Such a system can be analyzed at different complexity levels, from cognitive functions to molecular structure of ion channels. However, it remains extremely difficult to establish links between these different levels. An alternative strategy relies on the use of much simpler animals that can be easily manipulated. In 1974, S. Brenner introduced the nematode Caenorhabditis elegans as a model system. This worm has a simple nervous system that only contains 302 neurons and about 7,000 synapses. Forward genetic screens are powerful tools to identify genes required for specific neuron functions and behaviors. Moreover, studies of mutant phenotypes can identify the function of a protein in the nervous system. The data that have been obtained in C. elegans demonstrate a fascinating conservation of the molecular and cellular biology of the neuron between worms and mammals through more than 550 million years of evolution.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Neuropilin-1 Conveys Semaphorin and VEGF Signaling during Neural and Cardiovascular Development

            Neuropilin-1 (Npn-1) is a receptor that binds multiple ligands from structurally distinct families, including secreted semaphorins (Sema) and vascular endothelial growth factors (VEGF). We generated npn-1 knockin mice, which express an altered ligand binding site variant of Npn-1, and npn-1 conditional null mice to establish the cell-type- and ligand specificity of Npn-1 function in the developing cardiovascular and nervous systems. Our results show that VEGF-Npn-1 signaling in endothelial cells is required for angiogenesis. In striking contrast, Sema-Npn-1 signaling is not essential for general vascular development but is required for axonal pathfinding by several populations of neurons in the CNS and PNS. Remarkably, both Sema-Npn-1 signaling and VEGF-Npn-1 signaling are critical for heart development. Therefore, Npn-1 is a multifunctional receptor that mediates the activities of structurally distinct ligands during development of the heart, vasculature, and nervous system.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Collapsin: a protein in brain that induces the collapse and paralysis of neuronal growth cones.

              Repulsive guidance cues can steer neuronal growth cones during development and prevent mature axons from regenerating. We have identified a 100 kd glycoprotein in the chick brain that is a good candidate for a repulsive cue. Since it induces the collapse and paralysis of neuronal growth cones in vitro, we have named it collapsin. It is effective at concentrations of approximately 10 pM. The C-terminal half of collapsin contains a single immunoglobulin-like domain and an additional highly basic region. The N-terminal half of collapsin shares significant homology with fasciclin IV, a growth cone guidance protein in grasshopper. Recombinant collapsin causes sensory ganglion growth cones to collapse but not retinal ganglion cell growth cones. We propose that collapsin could serve as a ligand that guides specific growth cones by a motility-inhibiting mechanism.
                Bookmark

                Author and article information

                Journal
                Genetics
                Genetics
                Genetics Society of America
                0016-6731
                1943-2631
                November 07 2012
                November 2012
                November 2012
                August 31 2012
                : 192
                : 3
                : 959-971
                Article
                10.1534/genetics.112.144253
                3522169
                22942127
                © 2012

                Comments

                Comment on this article