Somatic motoneurone specification in the hindbrain: the influence of somite-derived signals, retinoic acid and Hoxa3

Guidato, Sonia; Prin, Fabrice; Guthrie, Sarah

doi:10.1242/dev.00496

Cited by 48 publications

(40 citation statements)

References 57 publications

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“…The truncated Robo1⌬-GFP and Robo2⌬-GFP transcripts consisted of the extracellular and transmembrane domain, but with the cytoplasmic domain deleted and a GFP tag substituted. Embryos were incubated to stages 17-19 and immunohistochemistry was performed as described previously (Guidato et al, 2003) using anti-SC1 (DSHB, USA; 1:10), anti-Myc (Autogen Bioclear, UK; 1:100), anti-islet1/2 (4D5, DSHB, USA; at 1:100) and anti-neurofilament H (1:600, Chemicon, UK). …”

Section: Electroporation Of Chick Embryos In Ovomentioning

confidence: 99%

Slit-mediated repulsion is a key regulator of motor axon pathfinding in the hindbrain

et al. 2005

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The floor plate is known to be a source of repellent signals for cranial motor axons, preventing them from crossing the midline of the hindbrain. However, it is unknown which molecules mediate this effect in vivo. We show that Slit and Robo proteins are candidate motor axon guidance molecules, as Robo proteins are expressed by cranial motoneurons, and Slit proteins are expressed by the tissues that delimit motor axon trajectories, i.e. the floor plate and the rhombic lip. We present in vitro evidence showing that Slit1 and Slit2 proteins are selective inhibitors and repellents for dorsally projecting, but not for ventrally projecting, cranial motor axons. Analysis of mice deficient in Slit and Robo function shows that cranial motor axons aberrantly enter the midline, while ectopic expression of Slit1 in chick embryos leads to specific motor axon projection errors. Expression of dominant-negative Robo receptors within cranial motoneurons in chick embryos strikingly perturbs their projections, causing some motor axons to enter the midline, and preventing dorsally projecting motor axons from exiting the hindbrain. These data suggest that Slit proteins play a key role in guiding dorsally projecting cranial motoneurons and in facilitating their neural tube exit.

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Section: Electroporation Of Chick Embryos In Ovomentioning

confidence: 99%

Slit-mediated repulsion is a key regulator of motor axon pathfinding in the hindbrain

et al. 2005

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“…In the spinal cord, for example, Hoxc8 and Hoxd10 are required for the normal development of motoneurons controlling movement of the forelimbs and hindlimbs, respectively (Carpenter et al, 1997;Tiret et al, 1998). In the hindbrain, Hoxb1 and Hox3 genes are necessary and sufficient for the specification of rhombomere (r) 4-branchial and r5-somatic motoneurons, respectively (Bell et al, 1999;Gaufo et al, 2000;Gaufo et al, 2003;Goddard et al, 1996;Guidato et al, 2003;Studer et al, 1996). These examples of motoneuron specification illustrate the phenomenon of spatial colinearity, whereby expression and function of Hox genes along the AP axis of the organism is correlated with their chromosomal location (Lewis, 1978;McGinnis and Krumlauf, 1992).…”

Section: Introductionmentioning

confidence: 99%

Contribution of Hox genes to the diversity of the hindbrain sensory system

Gaufo

Capecchi

2004

Development

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The perception of environmental stimuli is mediated through a diverse group of first-order sensory relay interneurons located in stereotypic positions along the dorsoventral (DV) axis of the neural tube. These interneurons form contiguous columns along the anteroposterior (AP) axis. Like neural crest cells and motoneurons, first-order sensory relay interneurons also require specification along the AP axis. Hox genes are prime candidates for providing this information. In support of this hypothesis, we show that distinct combinations of Hox genes in rhombomeres (r) 4 and 5 of the hindbrain are required for the generation of precursors for visceral sensory interneurons. As Hoxa2 is the only Hox gene expressed in the anterior hindbrain(r2), disruption of this gene allowed us to also demonstrate that the precursors for somatic sensory interneurons are under the control of Hox genes. Surprisingly, the Hox genes examined are not required for the generation of proprioceptive sensory interneurons. Furthermore, the persistence of some normal rhombomere characteristics in Hox mutant embryos suggests that the loss of visceral and somatic sensory interneurons cannot be explained solely by changes in rhombomere identity. Hox genes may thus directly regulate the specification of distinct first-order sensory relay interneurons within individual rhombomeres. More generally, these findings contribute to our understanding of how Hox genes specifically control cellular diversity in the developing organism

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“…Krox20 is required for the maintenance of r3 and r5 identity (Schneider-Maunoury et al, 1997) and cooperates with Kr to regulate hoxb3 directly in r5 (Manzanares et al, 2002). Furthermore, hox3 genes are both necessary and sufficient for the development of somatic motoneurons in the hindbrain (Gaufo et al, 2003;Guidato et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

vhnf1integrates global RA patterning and local FGF signals to direct posterior hindbrain development in zebrafish

et al. 2004

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The vertebrate hindbrain is transiently divided along the anterior-posterior axis into seven morphologically and molecularly distinct segments, or rhombomeres, that correspond to Hox expression domains. The establishment of a proper `hox code' is required for the development of unique rhombomere identities, including specification of neuronal fates. valentino (val), the zebrafish ortholog of mafB/Kreisler(Kr), encodes a bZip transcription factor that is required cell autonomously for the development of rhombomere (r) 5 and r6 and for activation of Hox group 3 gene expression. Recent work has demonstrated that the expression of val itself depends on three factors: retinoic acid (RA)signals from the paraxial mesoderm; fibroblast growth factor (Fgf) signals from r4; and variant hepatocyte nuclear factor 1 (vhnf1,also known as tcf2), a homeodomain transcription factor expressed posterior to the r4-5 boundary. We have investigated the interactions between these inputs onto val expression in the developing zebrafish hindbrain. We show that RA induces val expression via activation of vhnf1 expression in the hindbrain. Fgf signals from r4, acting through the MapK pathway, then cooperate with Vhnf1 to activate valexpression and subsequent r5 and r6 development. Additionally, vhnf1and val function as part of a multistep process required for the repression of r4 identity in the posterior hindbrain. vhnf1 acts largely independently of val to repress the r4 `hox code'posterior to the r4-5 boundary and therefore to block acquisition of r4-specific neuronal fates in the posterior hindbrain. However, vhnf1is not able to repress all aspects of r4 identity equivalently. valis required downstream of vhnf1 to repress r4-like cell-surface properties, as determined by an `Eph-ephrin code', by repressing ephrin-B2a expression in r5 and r6. The different requirements for vhnf1 and val to repress hoxb1a and ephrin-B2a, respectively, demonstrate that not all aspects of an individual rhombomere's identity are regulated coordinately.

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Somatic motoneurone specification in the hindbrain: the influence of somite-derived signals, retinoic acid and Hoxa3

Cited by 48 publications

References 57 publications

Slit-mediated repulsion is a key regulator of motor axon pathfinding in the hindbrain

Slit-mediated repulsion is a key regulator of motor axon pathfinding in the hindbrain

Contribution of Hox genes to the diversity of the hindbrain sensory system

vhnf1integrates global RA patterning and local FGF signals to direct posterior hindbrain development in zebrafish

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