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We study the cellular and molecular mechanisms regulating cell fate decisions at the neural plate border. In the vertebrate embryo, the neural plate border defines a competence domain established between neural (prospective central nervous system) and non-neural (future epidermis) ectoderm. Within this domain signaling events progressively direct the emergence of two cell populations, the neural crest and cranial placodes. In the head region the neural crest contributes to cartilages and bones of the face, the middle ear ossicles and several cranial ganglia. The cranial placodes form the paired sensory organs (olfactory epithelium, inner ear and lens), the adenohypophysis, and a subset of cranial ganglia including the trigeminal ganglion, which provides sensory innervation to the orofacial complex. Using Xenopus laevis as a model system, our goal is to identify the gene regulatory network driving neural crest and placode fates. Because neural crest and placode progenitors make a major contribution to the head structures and sensory organs, defining how these processes are regulated is essential to gain insights into the etiology and pathogenesis of congenital disorders affecting craniofacial development. The transcription Zic1 is expressed at the anterior neural plate, and we have recently shown that Zic1 controls cranial placode progenitors formation non-cell autonomously by regulating retinoic acid production and transport. We are now investigating how the balance between retinoic acid production and degradation contributes to the delineation of sharp boundaries of genes expression anteriorly, and characterizing the signaling molecules cooperating with retinoic acid to impart placode fate. Another line of research explores the role of components of the spliceosome in neural crest and craniofacial development. Several human craniofacial disorders have been linked to mutations in genes encoding proteins involved in pre-mRNA processing. We have developed the first animal model for Nager syndrome a craniofacial syndrome that has been linked to mutations in SF3B4 (splicing factor 3b, subunit 4) gene, which encodes a component of the spliceosomal complex. We have shown that in embryos lacking Sf3b4 function neural crest progenitors formation is compromised through a mechanism that involves increased apoptosis, resulting in hypo-plastic craniofacial skeletal structures. We are investigating the mechanisms by which Sf3b4 mediates its activity during neural crest formation by analyzing the global impact of Sf3b4 knockdown on pre-mRNA processing using RNA-Seq.
We study the cellular and molecular mechanisms regulating cell fate decisions at the neural plate border. In the vertebrate embryo, the neural plate border defines a competence domain established between neural (prospective central nervous system) and non-neural (future epidermis) ectoderm. Within this domain signaling events progressively direct the emergence of two cell populations, the neural crest and cranial placodes. In the head region the neural crest contributes to cartilages and bones of the face, the middle ear ossicles and several cranial ganglia. The cranial placodes form the paired sensory organs (olfactory epithelium, inner ear and lens), the adenohypophysis, and a subset of cranial ganglia including the trigeminal ganglion, which provides sensory innervation to the orofacial complex. Using Xenopus laevis as a model system, our goal is to identify the gene regulatory network driving neural crest and placode fates. Because neural crest and placode progenitors make a major contribution to the head structures and sensory organs, defining how these processes are regulated is essential to gain insights into the etiology and pathogenesis of congenital disorders affecting craniofacial development. The transcription Zic1 is expressed at the anterior neural plate, and we have recently shown that Zic1 controls cranial placode progenitors formation non-cell autonomously by regulating retinoic acid production and transport. We are now investigating how the balance between retinoic acid production and degradation contributes to the delineation of sharp boundaries of genes expression anteriorly, and characterizing the signaling molecules cooperating with retinoic acid to impart placode fate. Another line of research explores the role of components of the spliceosome in neural crest and craniofacial development. Several human craniofacial disorders have been linked to mutations in genes encoding proteins involved in pre-mRNA processing. We have developed the first animal model for Nager syndrome a craniofacial syndrome that has been linked to mutations in SF3B4 (splicing factor 3b, subunit 4) gene, which encodes a component of the spliceosomal complex. We have shown that in embryos lacking Sf3b4 function neural crest progenitors formation is compromised through a mechanism that involves increased apoptosis, resulting in hypo-plastic craniofacial skeletal structures. We are investigating the mechanisms by which Sf3b4 mediates its activity during neural crest formation by analyzing the global impact of Sf3b4 knockdown on pre-mRNA processing using RNA-Seq.
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AMERICAN JOURNAL OF MEDICAL GENETICS PART App.e63615-e63615, (2024)
bioRxiv : the preprint server for biology (2024)
DEVELOPMENTAL BIOLOGY (2024): 20-30
AMERICAN JOURNAL OF MEDICAL GENETICS PART Ano. 7 (2023): 1994-2002
Cells & development (2023): 203878-203878
Rahul Raghavan,Ugo Coppola,Yushi Wu,Chibuike Ihewulezi,Lenny J. Negrón-Piñeiro, Julie E. Maguire,Justin Hong,Matthew Cunningham,Han Jo Kim,Todd J. Albert,Abdullah M. Ali,Jean-Pierre Saint-Jeannet,
BMC ecology and evolutionno. 1 (2023): 1-22
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