<i>Drosophila</i>Plexin B is a Sema-2a receptor required for axon guidance

Ayoob, Joseph C.; Terman, Jonathan R.; Kolodkin, Alex L.

doi:10.1242/dev.02380

Cited by 76 publications

(125 citation statements)

References 45 publications

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“…ISNb axon guidance is qualitatively affected in the same way in sema1a, plexA, and plexB loss-of-function mutants. In all three mutants, ISNb fails to appropriately innervate its normal ventral muscle targets and instead continues to project dorsally with the ISN (an ISNb bypass phenotype) (Ayoob et al, 2006;Winberg et al, 1998b;Yu et al, 1998). Similarly, the individual misexpression of sema1a, plexA, and plexB also lead to ISNb bypass phenotypes or ISNb stall phenotypes that can be interpreted as bypass phenotypes (Winberg et al, 1998b;Yu et al, 1998;and this study).…”

Section: Discussionmentioning

confidence: 53%

“…Of the two Drosophila plexins, plexA has been shown to transduce transmembrane semaphorin signals while plexB transduces secreted semaphorin signals (Ayoob et al, 2006;Winberg et al, 1998b;Wu et al, 2011). A number of downstream signaling components have also been identified in Drosophila including off-track, Mical, Rac, nervy, and Gyc76C (Ayoob et al, 2004;Hu et al, 2001;Terman and Kolodkin, 2004;Terman et al, 2002;Winberg et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

“…Given that Sema-2b can bind PlexB and not PlexA , it is possible that signaling downstream of PlexB inhibits the PlexA pathway. Previous work has found that the two Plexin proteins physically interact and this could underlie such an inhibitory mechanism (Ayoob et al, 2006). Furthermore, Sema-2a protein has been shown to be transported down axons suggesting that it could be available to control signaling in the growth cone .…”

Section: Developmental Dynamicsmentioning

confidence: 99%

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Drosophila semaphorin2b is required for the axon guidance of a subset of embryonic neurons

Emerson

Long

Vactor

2013

Developmental Dynamics

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Background: The process of axon guidance is important in establishing functional neural circuits. The differential expression of cell-autonomous axon guidance factors is crucial for allowing axons of different neurons to take unique trajectories in response to spatially and temporally restricted cell non-autonomous axon guidance factors. A key motivation in the field is to provide adequate explanations for axon behavior with respect to the differential expression of these factors. Results: We report the characterization of a predicted secreted semaphorin family member, semaphorin2b (Sema-2b) in Drosophila embryonic axon guidance. Misexpression of Sema-2b in neurons causes highly penetrant axon guidance phenotypes in specific longitudinal and motoneuron pathways; however, expression of Sema-2b in muscles traversed by these motoneurons has no effect on axon guidance. In Sema-2b loss-of-function embryos, specific motoneuron and interneuron axon pathways display guidance defects. Specific visualization of the neurons that normally express Sema-2b reveals that this neuronal cohort is strongly affected by Sema-2b loss-offunction alleles. Conclusions: While secreted semaphorins have been implicated as cell non-autonomous chemorepellants in a variety of contexts, here we report previously undescribed Sema-2b loss-of-function and misexpression phenotypes that are consistent with a cell-autonomous role for Sema-2b. Developmental Dynamics 242:861-873, 2013. V C 2013 Wiley Periodicals, Inc.Key words: Drosophila; axon guidance; semaphorin Key Findings:Misexpression of the secreted semaphorin Sema-2b in neurons results in specific axon guidance phenotypes. Both Sema-2b loss-of-function and misexpression phenotypes are congruent with a cell-autonomous role for Sema-2b. Novel axon guidance phenotypes caused by Sema-2b loss-of-function mutations are characterized.

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Section: Discussionmentioning

confidence: 53%

Section: Discussionmentioning

confidence: 99%

Section: Developmental Dynamicsmentioning

confidence: 99%

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Drosophila semaphorin2b is required for the axon guidance of a subset of embryonic neurons

Emerson

Long

Vactor

2013

Developmental Dynamics

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“…Drosophila expresses two class 2 semaphorins, Sema-2a and Sema-2b; Sema 2a is expressed by muscles, where it acts as a repellent in motor axon targeting in the neuromuscular system (Winberg et al 1998). The Drosophila plexin PlexB has recently been shown to act as a receptor for Sema-2a (Ayoob et al 2006). In contrast to our findings in C. elegans, in Drosophila the plexB phenotype is much more severe than the Sema-2a phenotype, implying that PlexB interacts with additional ligands, possibly Sema-2b or itself.…”

Section: Discussionmentioning

confidence: 99%

The Plexin PLX-2 and the Ephrin EFN-4 Have Distinct Roles in MAB-20/Semaphorin 2A Signaling in Caenorhabditis elegans Morphogenesis

et al. 2007

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Semaphorins are extracellular proteins that regulate axon guidance and morphogenesis by interacting with a variety of cell surface receptors. Most semaphorins interact with plexin-containing receptor complexes, although some interact with non-plexin receptors. Class 2 semaphorins are secreted molecules that control axon guidance and epidermal morphogenesis in Drosophila and Caenorhabditis elegans. We show that the C. elegans class 2 semaphorin MAB-20 binds the plexin PLX-2. plx-2 mutations enhance the phenotypes of hypomorphic mab-20 alleles but not those of mab-20 null alleles, indicating that plx-2 and mab-20 act in a common pathway. Both mab-20 and plx-2 mutations affect epidermal morphogenesis during embryonic and in postembryonic development. In both contexts, plx-2 null mutant phenotypes are much less severe than mab-20 null phenotypes, indicating that PLX-2 is not essential for MAB-20 signaling. Mutations in the ephrin efn-4 do not synergize with mab-20, indicating that EFN-4 may act in MAB-20 signaling. EFN-4 and PLX-2 are coexpressed in the late embryonic epidermis where they play redundant roles in MAB-20-dependent cell sorting.

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“…In particular, repulsive signaling mediated by the Semaphorin-Plexin (Sema-Plex) pathway is essential for motor axon defasciculation (Ayoob et al, 2006;Terman et al, 2002;Winberg et al, 1998a;Yu et al, 2000). In wild-type embryos, axons of the intersegmental nerve branch b (ISNb) defasciculate from the primary ISN pathway and innervate the ventrolateral muscle (VLM) field.…”

Section: Introductionmentioning

confidence: 99%

Matrix metalloproteinases promote motor axon fasciculation in theDrosophilaembryo

2008

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Matrix metalloproteinases (MMPs) are a large conserved family of extracellular proteases, a number of which are expressed during neuronal development and upregulated in nervous system diseases. Primarily on the basis of studies using pharmaceutical inhibitors, MMPs have been proposed to degrade the extracellular matrix to allow growth cone advance during development and hence play largely permissive roles in axon extension. Here we show that MMPs are not required for axon extension in the Drosophila embryo, but rather are specifically required for the execution of several stereotyped motor axon pathfinding decisions. The Drosophila genome contains only two MMP homologs, Mmp1 and Mmp2. We isolated Mmp1 in a misexpression screen to identify molecules required for motoneuron development. Misexpression of either MMP inhibits the regulated separation/defasciculation of motor axons at defined choice points. Conversely, motor nerves in Mmp1 and Mmp2 single mutants and Mmp1 Mmp2 double mutant embryos are loosely bundled/fasciculated, with ectopic axonal projections. Quantification of these phenotypes reveals that the genetic requirement for Mmp1 and Mmp2 is distinct in different nerve branches, although generally Mmp2 plays the predominant role in pathfinding. Using both an endogenous MMP inhibitor and MMP dominantnegative constructs, we demonstrate that MMP catalytic activity is required for motor axon fasciculation. In support of the model that MMPs promote fasciculation, we find that the defasciculation observed when MMP activity is compromised is suppressed by otherwise elevating interaxonal adhesion -either by overexpressing Fas2 or by reducing Sema-1a dosage. These data demonstrate that MMP activity is essential for embryonic motor axon fasciculation.KEY WORDS: Drosophila melanogaster, Motoneuron, Motor axon pathfinding, Mmp1, Mmp2, Sema-1a, Fasciclin II, Timp Development 135, 95-109 (2008)

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DrosophilaPlexin B is a Sema-2a receptor required for axon guidance

Cited by 76 publications

References 45 publications

Drosophila semaphorin2b is required for the axon guidance of a subset of embryonic neurons

Drosophila semaphorin2b is required for the axon guidance of a subset of embryonic neurons

The Plexin PLX-2 and the Ephrin EFN-4 Have Distinct Roles in MAB-20/Semaphorin 2A Signaling in Caenorhabditis elegans Morphogenesis

Matrix metalloproteinases promote motor axon fasciculation in theDrosophilaembryo

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