Altered neuronal lineages in the facial ganglia of Hoxa2 mutant mice

Yang, Xiu Juan; Zhou, Yuefang; Barcarse, Erin A.; O’Gorman, Stephen

doi:10.1016/j.ydbio.2007.11.032

Cited by 12 publications

(12 citation statements)

References 295 publications

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“…Indeed, p53 is known to be mainly involved in cell cycle arrest, senescence and apoptosis [67]. Thus, a p53 stabilization would, at a first glance, induce cell cycle arrest, senescence and/or increase in apoptosis, which is not in line with Hoxa2 functional studies that led to postulate anti-differentiation and pro-proliferative roles for Hoxa2 [43,46,68]. Nevertheless, besides its role in cell cycle and apoptosis, p53 has also been involved in DNA repair.…”

Section: Discussionmentioning

confidence: 99%

The Homeodomain Transcription Factor Hoxa2 Interacts with and Promotes the Proteasomal Degradation of the E3 Ubiquitin Protein Ligase RCHY1

et al. 2013

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Hox proteins are conserved homeodomain transcription factors known to be crucial regulators of animal development. As transcription factors, the functions and modes of action (co-factors, target genes) of Hox proteins have been very well studied in a multitude of animal models. However, a handful of reports established that Hox proteins may display molecular activities distinct from gene transcription regulation. Here, we reveal that Hoxa2 interacts with 20S proteasome subunits and RCHY1 (also known as PIRH2), an E3 ubiquitin ligase that targets p53 for degradation. We further show that Hoxa2 promotes proteasome-dependent degradation of RCHY1 in an ubiquitin-independent manner. Correlatively, Hoxa2 alters the RCHY1-mediated ubiquitination of p53 and promotes p53 stabilization. Together, our data establish that Hoxa2 can regulate the proteasomal degradation of RCHY1 and stabilization of p53.

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Section: Discussionmentioning

confidence: 99%

The Homeodomain Transcription Factor Hoxa2 Interacts with and Promotes the Proteasomal Degradation of the E3 Ubiquitin Protein Ligase RCHY1

et al. 2013

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“…Fate mapping of rhombomere 4-derived neural crest using a Hoxb1-cre driver labels very few neurons of the geniculate ganglion, as identified by NeuN (Arenkiel et al, 2003) or Islet1/2 (Yang et al, 2008) expression. Remarkably, in Hoxa2 null mice, there is a marked increase in neural differentiation in neural crest-derived cells in the vicinity of the geniculate (Yang et al, 2008). In another study, Ap2α-Cre fate mapping of placode-derived cells frequently labeled geniculate neurons.…”

Section: Discussionmentioning

confidence: 99%

Hmx1 is required for the normal development of somatosensory neurons in the geniculate ganglion

Quina¹,

Tempest²,

Hsu³

et al. 2012

Developmental Biology

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Hmx1 is a variant homeodomain transcription factor expressed in the developing sensory nervous system, retina, and craniofacial mesenchyme. Recently, mutations at the Hmx1 locus have been linked to craniofacial defects in humans, rats, and mice, but its role in nervous system development is largely unknown. Here we show that Hmx1 is expressed in a subset of sensory neurons in the cranial and dorsal root ganglia which does not correspond to any specific sensory modality. Sensory neurons in the dorsal root and trigeminal ganglia of Hmx1dm/dm mouse embryos have no detectable Hmx1 protein, yet they undergo neurogenesis and express sensory subtype markers normally, demonstrating that Hmx1 is not globally required for the specification of sensory neurons from neural crest precursors. Loss of Hmx1 expression has no obvious effect on the early development of the trigeminal (V), superior (IX/X), or dorsal root ganglia neurons in which it is expressed, but results in marked defects in the geniculate (VII) ganglion. Hmx1dm/dm mouse embryos possess only a vestigial posterior auricular nerve, and general somatosensory neurons in the geniculate ganglion are greatly reduced by mid-gestation. Although Hmx1 is expressed in geniculate neurons prior to cell cycle exit, it does not appear to be required for neurogenesis, and the loss of geniculate neurons is likely to be the result of increased cell death. Fate mapping of neural crest-derived tissues indicates that Hmx1-expressing somatosensory neurons at different axial levels may be derived from either the neural crest or the neurogenic placodes.

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“…The NC also gives rise to postganglionic (PG) neurons of parasympathetic ganglia that are functional complements of epibranchial placode-derived visceral sensory ganglia associated with cranial nerves VII, IX, and X (D’Amico-Martel and Noden, 1983; Enomoto et al, 2000; Yang et al, 2008; Coppola et al, 2010; Takano-Maruyama et al, 2010; Chen et al, 2011) (Note that the ciliary ganglion associated with cranial nerve III is not included in this category because it is not associated with a complementary epibranchial placode-derived visceral sensory ganglion). Like the NC-derived precursors of the proximal ganglia, the NC-derived precursors of the parasympathetic ganglia are aligned with specific placodes along the AP axis (Takano-Maruyama et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Differential contribution of Neurog1 and Neurog2 on the formation of cranial ganglia along the anterior‐posterior axis

Takano-Maruyama

Chen

Gaufo

2011

Developmental Dynamics

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SUMMARY The neural crest (NC) and placode are transient neurogenic cell populations that give rise to cranial ganglia of the vertebrate head. The formation of the anterior NC- and placode-derived ganglia has been shown to depend on the single activity of either Neurog1 or Neurog2. The requirement of the more posterior cranial ganglia on Neurog1 and Neurog2 is unknown. Here we show that the formation of the NC-derived parasympathetic otic ganglia, and placode-derived visceral sensory petrosal and nodose ganglia are dependent on the redundant activities of Neurog1 and Neurog2. Tamoxifen-inducible Cre lineage labeling of Neurog1 and Neurog2 show a dynamic spatiotemporal expression profile in both NC and epibranchial placode that correlates with the phenotypes of the Neurog-mutant embryos. Our data, together with previous studies, suggest that the formation of cranial ganglia along the anterior-posterior axis is dependent on the dynamic spatiotemporal activities of Neurog1 and/or Neurog2 in both NC and epibranchial placode.

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Altered neuronal lineages in the facial ganglia of Hoxa2 mutant mice

Cited by 12 publications

References 295 publications

The Homeodomain Transcription Factor Hoxa2 Interacts with and Promotes the Proteasomal Degradation of the E3 Ubiquitin Protein Ligase RCHY1

The Homeodomain Transcription Factor Hoxa2 Interacts with and Promotes the Proteasomal Degradation of the E3 Ubiquitin Protein Ligase RCHY1

Hmx1 is required for the normal development of somatosensory neurons in the geniculate ganglion

Differential contribution of Neurog1 and Neurog2 on the formation of cranial ganglia along the anterior‐posterior axis

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