Genetic dissection of myelinated axons in zebrafish

Monk, Kelly R.; Talbot, William S.

doi:10.1016/j.conb.2009.08.006

Cited by 30 publications

(21 citation statements)

References 43 publications

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“…That is actually an important issue in the pathogenic mechanism of the disease because myelin cell function overtakes action potential conduction along peripheral axons (Monk and Talbot, 2009). In fact, the control of axoplasmic Ca 2+ and posttranslational modifications of local trafficking proteins are part of trophic support signaling provided by myelinating cells.…”

Section: Discussionmentioning

confidence: 99%

Deregulated expression of cytoskeleton related genes in the spinal cord and sciatic nerve of presymptomatic SOD1G93A Amyotrophic Lateral Sclerosis mouse model

Maximino

Oliveira

Alves

et al. 2014

Front. Cell. Neurosci.

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Early molecular events related to cytoskeleton are poorly described in Amyotrophic Lateral Sclerosis (ALS), especially in the Schwann cell (SC), which offers strong trophic support to motor neurons. Database for Annotation, Visualization and Integrated Discovery (DAVID) tool identified cytoskeleton-related genes by employing the Cellular Component Ontology (CCO) in a large gene profiling of lumbar spinal cord and sciatic nerve of presymptomatic SOD1G93A mice. One and five CCO terms related to cytoskeleton were described from the spinal cord deregulated genes of 40 days (actin cytoskeleton) and 80 days (microtubule cytoskeleton, cytoskeleton part, actin cytoskeleton, neurofilament cytoskeleton, and cytoskeleton) old transgene mice, respectively. Also, four terms were depicted from the deregulated genes of sciatic nerve of 60 days old transgenes (actin cytoskeleton, cytoskeleton part, microtubule cytoskeleton and cytoskeleton). Kif1b was the unique deregulated gene in more than one studied region or presymptomatic age. The expression of Kif1b [quantitative polymerase chain reaction (qPCR)] elevated in the lumbar spinal cord (40 days old) and decreased in the sciatic nerve (60 days old) of presymptomatic ALS mice, results that were in line to microarray findings. Upregulation (24.8 fold) of Kif1b was seen in laser microdissected enriched immunolabeled motor neurons from the spinal cord of 40 days old presymptomatic SOD1G93A mice. Furthermore, Kif1b was dowregulated in the sciatic nerve Schwann cells of presymptomatic ALS mice (60 days old) that were enriched by means of cell microdissection (6.35 fold), cell sorting (3.53 fold), and primary culture (2.70 fold) technologies. The gene regulation of cytoskeleton molecules is an important occurrence in motor neurons and Schwann cells in presymptomatic stages of ALS and may be relevant in the dying back mechanisms of neuronal death. Furthermore, a differential regulation of Kif1b in the spinal cord and sciatic nerve cells emerged as key event in ALS.

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Section: Discussionmentioning

confidence: 99%

Deregulated expression of cytoskeleton related genes in the spinal cord and sciatic nerve of presymptomatic SOD1G93A Amyotrophic Lateral Sclerosis mouse model

Maximino

Oliveira

Alves

et al. 2014

Front. Cell. Neurosci.

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“…The PLLn does not cross the basement membrane in Schwann cell-deficient mutants Sox10 is essential for the development of Schwann cells and other neural crest derivatives . In Schwann cells, ErbB2 and ErbB3 form a heteromeric receptor that is required for glial proliferation, migration and differentiation (Lyons et al, 2005;Monk and Talbot, 2009;Nave and Salzer, 2006). We have previously reported that in mutants lacking Schwann cells, including erbb2 st61 , erbb3 st48 and sox10 (cls t3 ) mutants, the PLLn is aberrantly localized in the epidermis at 3 dpf (Voas et al, 2009).…”

Section: Resultsmentioning

confidence: 99%

Schwann cells reposition a peripheral nerve to isolate it from postembryonic remodeling of its targets

2010

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SUMMARYAlthough much is known about the initial construction of the peripheral nervous system (PNS), less well understood are the processes that maintain the position and connections of nerves during postembryonic growth. Here, we show that the posterior lateral line nerve in zebrafish initially grows in the epidermis and then rapidly transitions across the epidermal basement membrane into the subepidermal space. Our experiments indicate that Schwann cells, which myelinate axons in the PNS, are required to reposition the nerve. In mutants lacking Schwann cells, the nerve is mislocalized and the axons remain in the epidermis. Transplanting wild-type Schwann cells into these mutants rescues the position of the nerve. Analysis of chimeric embryos suggests that the process of nerve relocalization involves two discrete steps -the degradation and recreation of the epidermal basement membrane. Although the outgrowth of axons is normal in mutants lacking Schwann cells, the nerve becomes severely disorganized at later stages. In wild-type embryos, exclusion of the nerve from the epidermis isolates axons from migration of their targets (sensory neuromasts) within the epidermis. Without Schwann cells, axons remain within the epidermis and are dragged along with the migrating neuromasts. Our analysis of the posterior lateral line system defines a new process in which Schwann cells relocate a nerve beneath the epidermal basement membrane to insulate axons from the postembryonic remodeling of their targets.

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“…That is, most of the critical molecular machinery of myelination is conserved between zebrafish and mammals (Monk and Talbot, 2009). Most important, the zebrafish model allows us to precisely study signaling mechanisms at the onset of myelination.…”

Section: Components Of the Canonical Wnt Signaling Pathway Drive Myelmentioning

confidence: 99%

“…Embryos were heat shocked at 2 dpf, corresponding to the onset of zebrafish myelination, whereby oligodendrocytes and Schwann cells start expressing myelin genes (Brosamle and Halpern, 2002;Lyons et al, 2005). mbp mRNA expression, a widely used marker for the onset of myelination in zebrafish (Monk and Talbot, 2009), was analyzed at 4 or 5 dpf by in situ hybridization at the level of the peripheral lateral line (PLLn), where axons are solely myelinated by Schwann cells.…”

Section: Interaction Between ␤-Catenin and Tcf3 Is Required For Schwamentioning

confidence: 99%

Wnt/β-Catenin Signaling Is an Essential and Direct Driver of Myelin Gene Expression and Myelinogenesis

Tawk¹,

Makoukji²,

Belle³

et al. 2011

J. Neurosci.

169

134

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Genetic dissection of myelinated axons in zebrafish

Cited by 30 publications

References 43 publications

Deregulated expression of cytoskeleton related genes in the spinal cord and sciatic nerve of presymptomatic SOD1G93A Amyotrophic Lateral Sclerosis mouse model

Deregulated expression of cytoskeleton related genes in the spinal cord and sciatic nerve of presymptomatic SOD1G93A Amyotrophic Lateral Sclerosis mouse model

Schwann cells reposition a peripheral nerve to isolate it from postembryonic remodeling of its targets

Wnt/β-Catenin Signaling Is an Essential and Direct Driver of Myelin Gene Expression and Myelinogenesis

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