Hoxa2 and Hoxb2 Control Dorsoventral Patterns of Neuronal Development in the Rostral Hindbrain

Davenne, Marc; Maconochie, Mark; Neun, Rüdiger; Pattyn, Alexandre; Chambon, Pierre; Krumlauf, Robb; Rijli, Filippo M.

doi:10.1016/s0896-6273(00)80728-x

Cited by 178 publications

(164 citation statements)

References 60 publications

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“…Interestingly, paralogous genes from different clusters have related AP expression domains but may respond to distinct dorsoventral patterning signals (Graham et al 1991;Davenne et al 1999). Recently, a functional relationship between Hox expression and MN specification was documented as HOXC6 and HOXC9 protein expression coincided with particular brachial and thoracic motoneurons (Dasen et al 2003).…”

Section: Mammalian Genomes Contain 39mentioning

confidence: 99%

HoxD cluster scanning deletions identify multiple defects leading to paralysis in the mouse mutant Ironside

Tarchini¹,

Huynh²,

Cox³

et al. 2005

Genes Dev.

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A spontaneous semidominant mutation (Ironside, Irn) was isolated in mice, leading to severe hindlimb paralysis following multiple deletions in cis at the HoxD locus. To understand its cellular and molecular etiology, we embarked on a comparative analysis using systematic HoxD cluster deletions, produced via targeted meiotic recombination (TAMERE). Different lines of mice were classified according to the severity of their paralyses, and subsequent analyses revealed that multiple causative factors were involved, alone or in combination, in the occurrence of this pathology. Among them are the loss of Hoxd10 function, the sum of remaining Hoxd gene activity, and the ectopic gain of function of the neighboring gene Evx2, all contributing to the mispositioning, the absence, or misidentification of specific lumbo-sacral pools of motoneurons, nerve root homeosis, and hindlimb innervation defects. These results highlight the importance of a systematic approach when studying such clustered gene families, and give insights into the function and regulation of Hox and Evx2 genes during early spinal cord development.[Keywords: Homeosis; peroneal nerve; chromosome engineering; motoneuron] Supplemental material is available at http://www.genesdev.org.

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Section: Mammalian Genomes Contain 39mentioning

confidence: 99%

HoxD cluster scanning deletions identify multiple defects leading to paralysis in the mouse mutant Ironside

Tarchini¹,

Huynh²,

Cox³

et al. 2005

Genes Dev.

View full text Add to dashboard Cite

show abstract

“…It seems that several other chick-specific, Krox20-dispensable processes start in r4 at the beginning of neuronal migration around HH12. Hox genes interact in r4 with neural specification programs to establish unique cell identities within each rhombomere (Davenne et al, 1999;Gaufo et al, 2000;Dasen et al, 2003;Pattyn et al, 2003). Rhombomere 4-specific phenotypic choices are made at this developmental stage, including the generation of branchiomotor versus serotonergic neurons (Pattyn et al, 2003) and the caudal migration of facial branchiomotor neurons through r5 and r6 (lacking in chicks) (Lumsden and Keynes, 1989;Pata et al, 1999;Garel et al, 2000;Gaufo et al, 2000;Studer, 2001).…”

Section: Development Of the Parafacial Rhythm Generator May Be Consermentioning

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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“…Whether PLZF À/À embryos display abnormalities in Hoxb2 expression in the developing CNS remains to be examined. However, the lack of obvious segmental defects in the CNS of PLZF null embryos is not surprising as Hoxb2 and Hoxa2 mutants themselves do not show r3/r5 defects (Gendron-Maguire et al, 1993;Rijli et al, 1993;Barrow and Capecchi, 1996;Davenne et al, 1999). It is likely that multiple factors regulate either different or overlapping programmes in the developing hindbrain.…”

Section: Cooperation Of Plzf With A/t-rich Motifsmentioning

confidence: 99%