2018
DOI: 10.1155/2018/8791304
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CRMP2 and CRMP4 Are Differentially Required for Axon Guidance and Growth in Zebrafish Retinal Neurons

Abstract: Axons are directed to their correct targets by guidance cues during neurodevelopment. Many axon guidance cues have been discovered; however, much less known is about how the growth cones transduce the extracellular guidance cues to intracellular responses. Collapsin response mediator proteins (CRMPs) are a family of intracellular proteins that have been found to mediate growth cone behavior in vitro; however, their roles in vivo in axon development are much less explored. In zebrafish embryos, we find that CRM… Show more

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Cited by 8 publications
(13 citation statements)
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“…Misregulation of sema3d alone does not, however, result in defects as intense as we observed, but rather in guidance errors of some RGC axons, leading to mixed ipsilateral and contralateral projections [28]. The same was shown after inactivation of other parts of Semaphorin signaling, including nrp1a, sema3e, adcy8, crmp4 and the sema-independent islr2 [27,45,55,56]. For rgmd, lrig1 and ephb2b, no mutant, KO or KD phenotype regarding RGC projections has been identified and they were not differentially regulated following Cyclopamine treatment.…”
Section: Discussionsupporting
confidence: 76%
“…Misregulation of sema3d alone does not, however, result in defects as intense as we observed, but rather in guidance errors of some RGC axons, leading to mixed ipsilateral and contralateral projections [28]. The same was shown after inactivation of other parts of Semaphorin signaling, including nrp1a, sema3e, adcy8, crmp4 and the sema-independent islr2 [27,45,55,56]. For rgmd, lrig1 and ephb2b, no mutant, KO or KD phenotype regarding RGC projections has been identified and they were not differentially regulated following Cyclopamine treatment.…”
Section: Discussionsupporting
confidence: 76%
“…Misregulation of sema3d alone does not, however, result in defects as intense as we observed, but rather in guidance errors of some RGC axons, leading to mixed ipsi-and contralateral projections (Sakai and Halloran, 2006). The same was shown after inactivation of other parts of Semaphorin signaling, including nrp1a, sema3e, adcy8, crmp4, and the sema-independent islr2 (Dell et al, 2013;Xu et al, 2010;Liu et al, 2018;Panza et al, 2015). For rgmd, lrig1, and ephb2b, no mutant, KO or KD phenotype regarding RGC projections has been identified and they were not differentially regulated following Cyclopamine treatment.…”
Section: Discussionsupporting
confidence: 72%
“…DPYSL2 knockout results in reduced dendritic spine density (Hiroko et al, 2016), and its dysfunction has been implicated in neurodevelopmental and psychiatric disorders with delayed onset, such as autism spectrum disorders and schizophrenia (Beasley et al, 2006;Hong et al, 2005). DPYSL2 is associated with neuronal microtubules and regulates axonal growth, and growth cone guidance (Liu et al, 2018;Hiroko et al, 2016). Brain slices from DPYSL2 knockout mice show abnormal long-term potentiation of synaptic transmission (Zhang et al, 2016), and behaviorally the mice exhibit increased locomotion, social, cognitive, and affective behavioral impairments (Zhang et al, 2016).…”
Section: Adev-il-10mentioning
confidence: 99%