Neuropilin 2/semaphorin 3F signaling is essential for cranial neural crest migration and trigeminal ganglion condensation

Gammill, Laura S.; González, Constanza; Bronner‐Fraser, Marianne

doi:10.1002/dneu.20326

Cited by 103 publications

(99 citation statements)

References 35 publications

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“…As shown in Table 2, many of the predicted targets of miRNAs whose expression changes upon exposure to the Notch inhibitor DAPT are involved in exactly these processes and further localize to the brain and neural crest (Wienholds et al, 2005). Specific examples of Notch signaling components that are predicted to be targets of one or more of the differentially expressed miRNAs shown in Figurer 3 and Table 2 include sema3fa (miR-204), which is necessary for neural crest migration (Gammill et al, 2006) as well as the glycoprotein gpm6ab (miR-29b), matrix metalloproteinase mmp14a (miR-29a), neuroepithelial polarity protein lin7a (miR-296), and the midbrain nucleolar protein, midnolin (miR-155).…”

Section: Mirna Expression Following Inhibition Of Hedgehog and Notch mentioning

confidence: 99%

MiRNA expression analysis during normal zebrafish development and following inhibition of the Hedgehog and Notch signaling pathways

Thatcher

Flynt

et al. 2007

Developmental Dynamics

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Section: Mirna Expression Following Inhibition Of Hedgehog and Notch mentioning

confidence: 99%

MiRNA expression analysis during normal zebrafish development and following inhibition of the Hedgehog and Notch signaling pathways

Thatcher

Flynt

et al. 2007

Developmental Dynamics

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“…Cells in the most anterior, or first, stream will migrate rostrally and caudally around the eye into the first pharyngeal arch and contribute to the jaw and palatal skeleton 5 . While research in zebrafish and amniotes have uncovered cues that regulate migration of cranial neural crest cells in all crest streams [25][26][27] , nothing is known of what cues specifically guide neural crest-derived palatal precursors to the first pharyngeal arch.Here, we show that Mirn140 attenuates Pdgf-mediated attraction during migration of neural crest-derived palatal precursors. Embryos injected with Mirn140 duplex and pdgfra mutants shared craniofacial phenotypes, including cleft palate and loss of oral ectoderm gene expression, suggesting an interaction between Mirn140 and pdgfra.…”

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confidence: 99%

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confidence: 99%

MicroRNA Mirn140 modulates Pdgf signaling during palatogenesis

et al. 2008

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Disruption of signaling pathways such as those mediated by Shh or Pdgf causes craniofacial disease, including cleft palate. The role that microRNAs play in modulating palatogenesis, however, is completely unknown. We show, in zebrafish, that the microRNA Mirn140 negatively regulates Pdgf signaling during palatal development and we provide a mechanism for how disruption of Pdgf signaling causes palatal clefting. The pdgf-receptor alpha (pdgfra) 3' UTR contains a Mirn140 binding site functioning in the negative regulation of Pdgfra protein levels in vivo. Both pdgfra mutants and Mirn140-injected embryos share panoply of facial defects including clefting of the crestderived cartilages that develop in the roof of the larval mouth. Concomitantly, the oral ectoderm beneath where these cartilages develop loses pitx2 and shha expression. Mirn140 modulates Pdgfmediated attraction of cranial neural crest cells to the oral ectoderm, where crest-derived signals are necessary for oral ectodermal gene expression. Both Mirn140 loss-of-function and pdgfra overexpression alters palatal shape and causes neural crest cells to accumulate around the optic stalk, a source of the ligand Pdgfaa. Conserved molecular genetics and expression patterns of mirn140 and pdgfra suggest that their regulatory interactions are ancient methods of palatogenesis that provide a candidate mechanism for cleft palate.Cleft palate and other craniofacial diseases are common in humans and have complex cellular and genetic etiologies. In amniotes, the palate serves to separate the nasal and oral cavities and is generated through an intricate series of morphogenic events that include early neural crest cell migration and cell-cell signaling during the formation of facial prominences, as well as later generation and fusion of palatal shelves. While later events involving palatal shelves have not been described in zebrafish, palatal precursors migrate both rostral and caudal to the eye to condense upon the oral ectoderm in amniotes 1 as well as zebrafish 2,3 and evidence continues to accumulate that the early signaling environment governing palatogenesis is also largely equivalent [3][4][5][6] . For instance, Hh signaling is crucial for palatogenesis in humans and zebrafish 3,4,7 . Zebrafish and amniotes also share expression patterns of palatogenic genes such as Shh 4,8 , Fgf8 4,9,10 and Pdgf receptor alpha (Pdgfra) [11][12][13] .In mouse, the Pdgf family consists of four soluble ligands, Pdgfa, Pdgfb, Pdgfc, and Pdgfd as well as two receptor tyrosine kinases, Pdgfra and Pdgfrb 14 . Pdgf signaling regulates a myriad of biological processes as demonstrated by analyses of mouse Pdgf ligand and receptor mutants 14 . Mice null for Pdgfra have a facial clefting phenotype that includes cleft palate 12,13 . This facial phenotype is fully recapitulated in mice doubly mutant for Pdgfa and Pdgfc 15. Most Pdgfc mutants have cleft palate 15 MicroRNAs (miRNAs) provide a unique mechanism for modulating signaling pathways [17][18][19][20] . Skeletogenic, including...

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“…In the head, a subset of cranial NCC emigrating from r4 are misguided anteriorly in Sema3a-and Nrp1-null mice, 52 and Sema3f-and Nrp2-null mutants exhibit mild migration defects in several cranial NCC populations. 53 Moreover, mutants lacking both pathways show fusion of the trigeminal and facial ganglia, and this leads to an intermingling of their sensory axons. 52 In the trunk, SEMA3A/NRP1 signaling controls the switch of NCC migration from an early path through the intersomitic furrows onto a major route through the anterior somites, 54 whereas SEMA3F/NRP2 signaling helps to restrict NCC migration to the anterior half of each somite.…”

Section: Discussionmentioning

confidence: 99%

“…52 In the trunk, SEMA3A/NRP1 signaling controls the switch of NCC migration from an early path through the intersomitic furrows onto a major route through the anterior somites, 54 whereas SEMA3F/NRP2 signaling helps to restrict NCC migration to the anterior half of each somite. 53 Because SEMA3A/NRP1 and SEMA3F/NRP2 signaling control distinct aspects of NCC guidance, mutants deficient in both pathways display severe defects in NCC guidance that lead to fusion of the dorsal root ganglia. 55,56 The signaling co-receptors for NRP1 and NRP2 in semaphorinmediated NCC guidance have not yet been identified, but they are not PLXNA3 or PLXNA4.…”

Section: Discussionmentioning

confidence: 99%