Progressive Spatial Restriction ofSek-1andKrox-20Gene Expression during Hindbrain Segmentation

Irving, Carol; Nieto, M. Ángela; DasGupta, Ruchira; Charnay, Patrick; Wilkinson, David G.

doi:10.1006/dbio.1996.0004

Cited by 115 publications

(65 citation statements)

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“…Krox20 expression starts in r3 as early as at HH8, before the onset of hindbrain segmentation (Nieto et al, 1991;Irving et al, 1996;Giudicelli et al, 2001). However, we show that several hours later, at HH10, induction of the episodic activity is blocked in a variety of rhombomeric configurations but can be restored by Krox20 electroporation.…”

Section: Discussionmentioning

confidence: 99%

Induction of a Parafacial Rhythm Generator by Rhombomere 3 in the Chick Embryo

Coutinho¹,

Borday²,

Gilthorpe³

et al. 2004

J. Neurosci.

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Observations of knock-out mice suggest that breathing at birth requires correct development of a specific hindbrain territory corresponding to rhombomeres (r) 3 and 4. Focusing on this territory, we examined the development of a neuronal rhythm generator in the chick embryo. We show that rhythmic activity in r4 is inducible after developmental stage 10 through interaction with r3. Although the nature of this interaction remains obscure, we find that the expression of Krox20, a segmentation gene responsible for specifying r3 and r5, is sufficient to endow other rhombomeres with the capacity to induce rhythmic activity in r4. Induction is robust, because it can be reproduced with r2 and r6 instead of r4 and with any hindbrain territory that normally expresses Krox20 (r3, r5) or can be forced to do so (r1, r4). Interestingly, the interaction between r4 and r3/r5 that results in rhythm production can only take place through the anterior border of r4, revealing a heretofore unsuspected polarity in individual rhombomeres. The r4 rhythm generator appears to be homologous to a murine respiratory parafacial neuronal system developing in r4 under the control of Krox20 and Hoxa1. These results identify a late role for Krox20 at the onset of neurogenesis.

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Section: Discussionmentioning

confidence: 99%

Induction of a Parafacial Rhythm Generator by Rhombomere 3 in the Chick Embryo

Coutinho¹,

Borday²,

Gilthorpe³

et al. 2004

J. Neurosci.

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“…Ephrin-B3͞Fc was preclustered by incubation with anti-human Fc␥ (Jackson Immunoresearch), a necessary step to activate the biological activity of ephrin Fc proteins. Cultures were grown for 2 days in Neurobasal A͞B27 medium, fixed, and immunolabeled with anti-acetylated tubulin (Sigma; to visualize neurites) and an antibody against the intracellular domain of EphA4 (anti-Sek i ; for cortical cells only) graciously provided by D. Wilkinson (22), or with anti-phosphotyrosine (Upstate Biotechnology) and anti-Sek i . Total neurite lengths from individual cerebellar and EphA4-positive cortical neurons were quantitated by using METAMORPH imaging software (Universal Imaging, Downingtown, PA) for 255-467 neurons per condition from duplicate or quadruplicate wells per experiment, and from at least three separate experiments.…”

Section: Methodsmentioning

confidence: 99%

Ephrin-B3 is a myelin-based inhibitor of neurite outgrowth

Benson

Romero

Lush

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

276

191

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The inability of CNS axons to regenerate after traumatic spinal cord injury is due, in part, to the inhibitory effects of myelin. The three major previously identified constituents of this activity (Nogo, myelin-associated glycoprotein, and oligodendrocyte myelin glycoprotein) were isolated based on their potent inhibition of axon outgrowth in vitro. All three myelin components transduce their inhibitory signals through the same Nogo receptor͞p75 neurotrophin receptor͞LINGO-1 (NgR1͞p75͞LINGO-1) complex. In this study, we considered that molecules known to act as repellants in vertebrate embryonic axonal pathfinding may also inhibit regeneration. In mice, ephrin-B3 functions during development as a midline repellant for axons of the corticospinal tract. We therefore investigated whether this repellant was expressed in the adult spinal cord and retained inhibitory activity. We demonstrate that ephrin-B3 is expressed in postnatal myelinating oligodendrocytes and, by using primary CNS neurons, show that ephrin-B3 accounts for an inhibitory activity equivalent to that of the other three myelin-based inhibitors, acting through p75, combined. Our data describe a known vertebrate axon guidance molecule as a myelinbased inhibitor of neurite outgrowth.spinal cord injury ͉ regeneration ͉ axon ͉ Eph receptor T he corticospinal tract (CST) is the major spinal axon bundle responsible for fine locomotor control. Damage to this tract contributes to the permanent loss of motor control that is the most visible hallmark of spinal cord injury (SCI). These, and other axons of the CNS damaged in SCI, do not regenerate, in part, because of the nonpermissive environment of myelin in the mature CNS (1). Constituents of this repressive activity in myelin include Nogo, myelin-associated glycoprotein (MAG), and oligodendrocyte myelin glycoprotein (OMgp) (reviewed in ref.2). The recently identified Nogo receptor (NgR1) is a glycosylphosphatidylinositol-linked molecule that binds the 66-aa extracellular loop of Nogo (Nogo-66) and transduces its inhibitory activity when expressed in neurons (3). Surprisingly, MAG and OMgp also bind the NgR1 (4-6) in a complex with the p75 neurotrophin receptor and the newly characterized leucine rich repeat transmembrane protein LINGO-1. p75 and LINGO-1 are requisite signaling components for inhibition by Nogo-66, MAG, and OMgp as p75 Ϫ/Ϫ cerebellar granule neurons (CGNs) or dorsal root ganglion (DRG) neurons exhibit reduced sensitivity to these three inhibitors and to inhibition by CNS myelin (7), and NgR1͞p75 complexes confer sensitivity to these inhibitors only in the presence of LINGO-1 (8).Although it is thought that Nogo, MAG, and OMgp may act in the uninjured CNS to control aberrant sprouting and stabilize mature connections (9), their normal and developmental roles remain a mystery. Axon repellants such as semaphorins, slits, and ephrins play critical roles in tract formation during embryonic development (10). We previously proposed that such molecules may function as inhibitors of regeneration in the...

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“…Embryos were fixed in 4% paraformaldehyde, and immunohistochemistry was performed as previously described (Prince et al, 1998) using the following primary antibodies: EphA4 [generous gift from David Wilkinson (Irving et al, 1996)] and REST (Abcam, ab21635).…”

Section: Immunohistochemistrymentioning

confidence: 99%

Zebrafish Prickle1b mediates facial branchiomotor neuron migration via a farnesylation-dependent nuclear activity

et al. 2011

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SUMMARYThe facial branchiomotor neurons (FBMNs) undergo a characteristic tangential migration in the vertebrate hindbrain. We previously used a morpholino knockdown approach to reveal that zebrafish prickle1b (pk1b) is required for this migration. Here we report that FBMN migration is also blocked in a pk1b mutant with a disruption in the consensus farnesylation motif. We confirmed that this lipid modification is required during FBMN migration by disrupting the function of farnesyl biosynthetic enzymes. Furthermore, farnesylation of a tagged Pk1b is required for its nuclear localization. Using a unique rescue approach, we have demonstrated that Pk1b nuclear localization and farnesylation are required during FBMN migration. Our data suggest that Pk1b acts at least partially independently of core planar cell polarity molecules at the plasma membrane, and might instead be acting at the nucleus. We also found that the neuronal transcriptional silencer REST is necessary for FBMN migration, and we provide evidence that interaction between Pk1b and REST is required during this process. Finally, we demonstrate that REST protein, which is normally localized in the nuclei of migrating FBMNs, is depleted from the nuclei of Pk1b-deficient neurons. We conclude that farnesylation-dependent nuclear localization of Pk1b is required to regulate REST localization and thus FBMN migration.

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Progressive Spatial Restriction ofSek-1andKrox-20Gene Expression during Hindbrain Segmentation

Cited by 115 publications

References 0 publications

Induction of a Parafacial Rhythm Generator by Rhombomere 3 in the Chick Embryo

Induction of a Parafacial Rhythm Generator by Rhombomere 3 in the Chick Embryo

Ephrin-B3 is a myelin-based inhibitor of neurite outgrowth

Zebrafish Prickle1b mediates facial branchiomotor neuron migration via a farnesylation-dependent nuclear activity

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