The Cell Adhesion Molecule L1 Is Required for Chain Migration of Neural Crest Cells in the Developing Mouse Gut

Anderson, Richard B.; Turner, Kirsty; Nikonenko, Alexander G.; Hemperly, John J.; Schachner, Melitta; Young, Heather M.

doi:10.1053/j.gastro.2006.01.002

Cited by 90 publications

(108 citation statements)

References 57 publications

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“…21 Third, L1CAM is expressed exclusively by neural crestderived cells in the developing mouse gut and L1CAM-deficient mice showed a small but significant reduction in enteric neural crest cell migration throughout the developing gut. 22 Although these observations suggest an important role for L1CAM in the migration of neural crest cells in the developing gut, the low incidence of HSCR disease in patients with L1CAM mutations (about 3%) and the absence of L1CAM mutations in males affected with isolated HSCR suggest that L1CAM is not an HSCR causative gene but provides a predisposing genetic background, likely acting as an X-linked modifier gene for the development of HSCR. 7 -9 Additional factors may act on this background promoting the occurrence of Hirschsprung's disease, among which the RET predisposing haplotype, found in our infant affected with HSCR and hydrocephalus and carrying a L1CAM mutation.…”

Section: Discussionmentioning

confidence: 98%

Complex pathogenesis of Hirschsprung's disease in a patient with hydrocephalus, vesico-ureteral reflux and a balanced translocation t(3;17)(p12;q11)

Griseri¹,

Vos

Giorda

et al. 2008

Eur J Hum Genet

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Hirschsprung's disease (HSCR), a congenital complex disorder of intestinal innervation, is often associated with other inherited syndromes. Identifying genes involved in syndromic HSCR cases will not only help understanding the specific underlying diseases, but it will also give an insight into the development of the most frequent isolated HSCR. The association between hydrocephalus and HSCR is not surprising as a large number of patients have been reported to show the same clinical association, most of them showing mutations in the L1CAM gene, encoding a neural adhesion molecule often involved in isolated X-linked hydrocephalus. L1 defects are believed to be necessary but not sufficient for the occurrence of the intestinal phenotype in syndromic cases. In this paper, we have carried out the molecular characterization of a patient affected with Hirschsprung's disease and X-linked hydrocephalus, with a de novo reciprocal balanced translocation t(3;17)(p12;q21). In particular, we have taken advantage of this chromosomal defect to gain access to the predisposing background possibly leading to Hirschsprung's disease. Detailed analysis of the RET and L1CAM genes, and molecular characterization of MYO18A and TIAF1, the genes involved in the balanced translocation, allowed us to identify, besides the L1 mutation c.2265delC, different additional factors related to RET-dependent and -independent pathways which may have contributed to the genesis of enteric phenotype in the present patient.

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Section: Discussionmentioning

confidence: 98%

Complex pathogenesis of Hirschsprung's disease in a patient with hydrocephalus, vesico-ureteral reflux and a balanced translocation t(3;17)(p12;q11)

Griseri¹,

Vos

Giorda

et al. 2008

Eur J Hum Genet

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“…Our work in Manduca has shown that many of the same classes of guidance cues involved in controlling neural crest cell migration also regulate the pathways chosen by the EP cells, including immunoglobulin-related cell adhesion receptors (Wright and Copenhaver, 2000;Yoneda et al, 2001;Anderson et al, 2006) and integrins (Breau et al, 2006;Coate & Copenhaver, unpublished data). While Ephrin-Eph receptor interactions play a prominent role in controlling the migration of trunk neural crest cells (Krull 2001), whether they also help guide crest-derived enteric neurons has not been comprehensively explored.…”

Section: A Possible Role For Msephrin-mseph Receptor Interactions In mentioning

confidence: 99%

Eph receptor expression defines midline boundaries for ephrin‐positive migratory neurons in the enteric nervous system of Manduca sexta

Coate

Swanson

Proctor

et al. 2007

J of Comparative Neurology

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Eph receptor tyrosine kinases and their ephrin ligands participate in the control of neuronal growth and migration in a variety of contexts, but the mechanisms by which they guide neuronal motility are still incompletely understood. Using the enteric nervous system (ENS) of the tobacco hornworm Manduca sexta as a model system, we have explored whether Manduca ephrin (MsEphrin; a GPIlinked ligand) and its Eph receptor (MsEph) may regulate the migration and outgrowth of enteric neurons. During the formation of the Manduca ENS, an identified set of ~300 neurons (EP cells) populate the enteric plexus of the midgut by migrating along a specific set of muscle bands that form on the gut, while they strictly avoid adjacent interband regions. By determining the mRNA and protein expression patterns for MsEphrin and the MsEph receptor and by examining their endogenous binding patterns within the ENS, we have demonstrated that the ligand and its receptor are distributed in a complementary manner: MsEphrin is exclusively expressed by the migratory EP cells, while the MsEph receptor is expressed by a discrete set of midline interband cells that are normally inhibitory to migration. Notably, MsEphrin could be detected on the filopodial processes of the EP cells that extended up to but not across the midline cells expressing the MsEph receptor. These results suggest a model whereby MsEphrin-dependent signaling regulates the response of migrating neurons to a midline inhibitory boundary, defined by the expression of MsEph receptors in the developing ENS.

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“…L1 has been shown to play a role in cell migration, synaptogenesis, synaptic plasticity, learning and memory, myelination, axon outgrowth and pathfinding, axon fasciculation and growth cone morphology (Dahme et al, 1997;Cohen et al, 1998;Demyanenko et al, 1999;Ourednik et al, 2001;Thelen et al, 2002;Law et al, 2003;Roonprapunt et al, 2003;Adcock et al, 2004;Saghatelyan et al, 2004;Anderson et al, 2006b;Maness and Schachner, 2007). L1 has also been reported to promote neuronal differentiation and inhibit glial cell differentiation of neural precursor cells in vitro (Dihne et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

“…We have recently shown that enteric neural crest-derived cells express L1 as they migrate within the developing gut, and that L1 is required for the chain migration of neural crest-derived cells within the gut (Anderson et al, 2006b). In the current study, we examined whether there were any changes in the proliferation, cell death or differentiation of neural crest-derived cells in the gut of mid-late embryonic and postnatal L1-deficient mice.…”

Section: Introductionmentioning

confidence: 99%

Cell adhesion molecule L1 affects the rate of differentiation of enteric neurons in the developing gut

Turner

Schachner

Anderson

2009

Developmental Dynamics

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The enteric nervous system arises predominantly from vagal level neural crest cells that migrate into and along the developing gut. As the neural crest-derived cells migrate within the gut, a subpopulation begins to differentiate into enteric neurons. Here, we show that the differentiation of neural crest-derived cells into enteric neurons is delayed in L1-deficient mice, compared with littermate controls. However, glial cell differentiation is not affected in L1-deficient mice. These mice also show a delay in the differentiation of a neurotransmitter-specific subtype of enteric neuron within the gastrointestinal tract. Together, these results suggest a role for the cell adhesion molecule, L1, in the differentiation of neural crestderived cells into enteric neurons within the developing enteric nervous system. Developmental Dynamics 238:708 -715, 2009.

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The Cell Adhesion Molecule L1 Is Required for Chain Migration of Neural Crest Cells in the Developing Mouse Gut

Cited by 90 publications

References 57 publications

Complex pathogenesis of Hirschsprung's disease in a patient with hydrocephalus, vesico-ureteral reflux and a balanced translocation t(3;17)(p12;q11)

Complex pathogenesis of Hirschsprung's disease in a patient with hydrocephalus, vesico-ureteral reflux and a balanced translocation t(3;17)(p12;q11)

Eph receptor expression defines midline boundaries for ephrin‐positive migratory neurons in the enteric nervous system of Manduca sexta

Cell adhesion molecule L1 affects the rate of differentiation of enteric neurons in the developing gut

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