Integrity of Developing Spinal Motor Columns Is Regulated by Neural Crest Derivatives at Motor Exit Points

Vermeren, Matthieu; Maro, Géraldine S.; Bron, Romke; McGonnell, Imelda M.; Charnay, Patrick; Topilko, Piotr; Cohen, J.A.

doi:10.1016/s0896-6273(02)01188-1

Cited by 121 publications

(169 citation statements)

References 43 publications

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“…Furthermore, vitamin A signaling has been shown to play an essential role in the development of many of these regions or associated structures in the vertebrate embryo (Helms et al, 1996;Stratford et al, 1996;Anchan et al, 1997;White et al, 1998White et al, , 2000Malpel et al, 2000;Mercader et al, 2000;Niederreither et al, 2000Niederreither et al, , 2002bBatourina et al, 2001;Dupé and Lumsden, 2001;Chazaud et al, 2003;Halilagic et al, 2003;Wilson et al, 2003). The expression of NEDD9 in the boundary cap cells of the dorsal root ganglion is intriguing in light of the proposed role of these cells in enabling axons unhindered access to the developing spinal cord while prohibiting the mixing of cells between emerging central nervous system and peripheral nervous system compartments (Vermeren et al, 2003). Boundary cap cells are also present at the future site of branchiomotor nerve exit points (Niederlä nder and Lumsden, 1996), and vitamin A is essential for normal development of the cranial nerves (White et al, 1998(White et al, , 2000.…”

Section: Discussionmentioning

confidence: 99%

Crk‐associated substrate (Cas) family member, NEDD9, is regulated in human neuroblastoma cells and in the embryonic hindbrain by all‐trans retinoic acid

Merrill

See

Wertheim

et al. 2004

Developmental Dynamics

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The vitamin A metabolite, all-trans retinoic acid (atRA), plays an essential role in vertebrate embryogenesis, including development of the nervous system. In the human neuroblastoma cell line, SH-SY5Y, atRA rapidly induces (within 4 hr) the expression of the Crk-associated substrate (Cas) family member, neural precursor cell-expressed, developmentally down-regulated gene 9 (NEDD9) also called the human enhancer of filamentation (HEF1). NEDD9 is expressed in the developing hindbrain (5-somite stage) in the presumptive rhombomeres 2, 3, and 5 before the onset of overt segmentation. Exposure of rat embryos to excess atRA at times ranging from E9.25 to E12 leads to altered NEDD9 expression in the developing hindbrain within 6 hr. NEDD9 expression is also perturbed in vitamin A-deficient embryos. A putative retinoic acid response element in the 5 region of the NEDD9 promoter binds specifically to a RXR/RAR heterodimer and forms a higher molecular weight complex upon addition of a retinoic acid receptorspecific antibody. Regulation of NEDD9 may be an important means whereby atRA promotes cell spreading and neurite outgrowth in SH-SY5Y human neuroblastoma cells, and NEDD9 represents a new downstream target of atRA and its receptors in the developing hindbrain. Developmental Dynamics 231:564 -575, 2004.

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Section: Discussionmentioning

confidence: 99%

Crk‐associated substrate (Cas) family member, NEDD9, is regulated in human neuroblastoma cells and in the embryonic hindbrain by all‐trans retinoic acid

Merrill

See

Wertheim

et al. 2004

Developmental Dynamics

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“…All mouse lines used in this study were maintained in a mixed C57BL/6/DBA2 background. We used the following alleles or transgenes that were genotyped as indicated in the original publications: Krox20 Soriano, 1999;Voiculescu et al, 2000;Ahn et al, 2001;Srinivas et al, 2001;Taillebourg et al, 2002;Pietri et al, 2003;Vermeren et al, 2003). All animal manipulations were performed according to French and European Union regulations.…”

Section: Methodsmentioning

confidence: 99%

“…For this purpose, we took advantage of a knock-in allele, Krox20 GFP(DT) , in which the Krox20 coding sequence has been replaced by a cassette containing the GFP coding sequence, flanked by loxP sites and followed by the coding sequence for the A chain of the diphtheria toxin (Vermeren et al, 2003). In this configuration, when the Krox20 locus is activated, only the GFP gene is expressed.…”

Section: Generation Of a Mouse Mutant Depleted Of Schwann And Bc Cellsmentioning

confidence: 99%

“…We have shown previously that BC cells participate in the maintenance of the integrity of the CNS/PNS border in birds and mammals, because BC cell ablation results in the emigration of motoneuron cell bodies into the PNS (Vermeren et al, 2003). However, the mechanisms maintaining the segregation between central and peripheral glia are not known.…”

Section: Introductionmentioning

confidence: 99%

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CNS/PNS Boundary Transgression by Central Glia in the Absence of Schwann Cells or Krox20/Egr2 Function

Coulpier¹,

Decker²,

Funalot³

et al. 2010

J. Neurosci.

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“…The importance of MHCIIB in generating the traction force that allows growth cone extension (Bridgman et al, 2001) suggests that this force might be increased in the absence of MLCP activity. There is a precedent for the idea that axon outgrowth can exert a pulling force on the cell body, because it has been shown that chick motor neurons will migrate out of the spinal cord along their axons if their movement is not blocked by boundary cap cells (Vermeren et al, 2003).…”

Section: Mbs Prevents Loss Of Photoreceptors From the Eye Disc Epithementioning

confidence: 99%

Excessive Myosin Activity inMbsMutants Causes Photoreceptor Movement Out of theDrosophilaEye Disc Epithelium

Lee

Treisman

2004

MBoC

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Neuronal cells must extend a motile growth cone while maintaining the cell body in its original position. In migrating cells, myosin contraction provides the driving force that pulls the rear of the cell toward the leading edge. We have characterized the function of myosin light chain phosphatase, which down-regulates myosin activity, in Drosophila photoreceptor neurons. Mutations in the gene encoding the myosin binding subunit of this enzyme cause photoreceptors to drop out of the eye disc epithelium and move toward and through the optic stalk. We show that this phenotype is due to excessive phosphorylation of the myosin regulatory light chain Spaghetti squash rather than another potential substrate, Moesin, and that it requires the nonmuscle myosin II heavy chain Zipper. Myosin binding subunit mutant cells continue to express apical epithelial markers and do not undergo ectopic apical constriction. In addition, mutant cells in the wing disc remain within the epithelium and differentiate abnormal wing hairs. We suggest that excessive myosin activity in photoreceptor neurons may pull the cell bodies toward the growth cones in a process resembling normal cell migration. INTRODUCTIONThe cytoskeleton plays a variety of roles during development, allowing cells to change their shape, adhesive properties, and motility (Jamora and Fuchs, 2002). Two critical components of the cytoskeleton are actin and nonmuscle myosin II. The contractile activity of actomyosin complexes has been implicated in cell migration, epithelial sheet movements, cytokinesis, axon outgrowth, and cell adhesion (Maciver, 1996;Jacinto et al., 2002;Dent and Gertler, 2003). During migration of several cell types, myosin activity is required to retract the rear of the cell (Ridley et al., 2003).Nonmuscle myosin II consists of a hexamer of two myosin heavy chains (MHC), two myosin light chains (MLC), and two myosin regulatory light chains (MRLC) (Korn and Hammer, 1988). Phosphorylation of key serine and threonine residues on MRLC stimulates the ATPase activity of MHC and promotes its assembly into filaments, leading to stress fiber contraction (Adelstein and Conti, 1975;Craig et al., 1983;Umemoto et al., 1989;Katoh et al., 2001). Mutations in the Drosophila orthologs of these myosin subunits have provided insight into the developmental functions of myosin II. Mutations in zipper (zip), which encodes MHC, cause defects in cytokinesis, closure of the dorsal embryonic epidermis over the amnioserosa, axon patterning, and myofibril formation (Zhao et al., 1988;Young et al., 1993;Bloor and Kiehart, 2001). spaghetti squash (sqh), encoding MRLC, is required for cytokinesis, oogenesis, and imaginal disc eversion (Karess et al., 1991;Wheatley et al., 1995;Edwards and Kiehart, 1996;Jordan and Karess, 1997).Actin-binding proteins of the ezrin, radixin, and moesin (ERM) family are thought to link transmembrane proteins to the actin cytoskeleton (Bretscher, 1999). ERM proteins are activated by phosphorylation of a conserved threonine residue, which inhibits associati...

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Integrity of Developing Spinal Motor Columns Is Regulated by Neural Crest Derivatives at Motor Exit Points

Cited by 121 publications

References 43 publications

Crk‐associated substrate (Cas) family member, NEDD9, is regulated in human neuroblastoma cells and in the embryonic hindbrain by all‐trans retinoic acid

Crk‐associated substrate (Cas) family member, NEDD9, is regulated in human neuroblastoma cells and in the embryonic hindbrain by all‐trans retinoic acid

CNS/PNS Boundary Transgression by Central Glia in the Absence of Schwann Cells or Krox20/Egr2 Function

Excessive Myosin Activity inMbsMutants Causes Photoreceptor Movement Out of theDrosophilaEye Disc Epithelium

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