Differential Shh, Bmp and Wnt gene expressions during craniofacial development in mice

Paiva, Katiúcia Batista Silva; Silva‐Valenzuela, Maria das Graças da; Massironi, Sílvia Maria Gomes; Ko, Gui Mi; Modolo, Filipe; Nunes, Fábio Daumas

doi:10.1016/j.acthis.2009.05.007

Cited by 30 publications

(20 citation statements)

References 48 publications

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“…This gene was also associated with nonsyndromic clefts in the Hispanic population described in Chiquet et al (2008). During craniofacial development, Wnt5A signals were detected in the mesenchymal cells and around Meckel’s cartilage and in only in the mesenchyme of the elevating palatal shelves (Paiva et al, 2009). …”

Section: Discussionmentioning

confidence: 99%

Studies with Wnt genes and nonsyndromic cleft lip and palate

Menezes

Letra

Kim

et al. 2010

Birth Defects Research

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Background-Clefts of the lip and/or palate (cleft lip/palate) are notable for their complex etiology. The WNT pathway regulates multiple developmental processes including craniofacial development and may play a role in cleft lip/palate and other defects of craniofacial development such as tooth agenesis. Variations in WNT genes have been recently associated with cleft lip/ palate in humans. In addition, two WNT genes, Wnt3 and Wnt9B, are located in the clf1 cleft locus in mice.

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Section: Discussionmentioning

confidence: 99%

Studies with Wnt genes and nonsyndromic cleft lip and palate

Menezes

Letra

Kim

et al. 2010

Birth Defects Research

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“…Sonic hedgehog (Shh) is expressed in the epithelium throughout palatogenesis (Paiva et al, 2010) and proper regulation of the Shh signal is crucial for normal palate development to occur. Expression is restricted to a striped pattern that corresponds to the rugae (Rice et al, 2006).…”

Section: Sonic Hedgehog Signalingmentioning

confidence: 99%

Molecular signaling along the anterior–posterior axis of early palate development

Smith¹,

Lozanoff²,

Iyyanar³

et al. 2013

Front. Physio.

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Cleft palate is a common congenital birth defect in humans. In mammals, the palatal tissue can be distinguished into anterior bony hard palate and posterior muscular soft palate that have specialized functions in occlusion, speech or swallowing. Regulation of palate development appears to be the result of distinct signaling and genetic networks in the anterior and posterior regions of the palate. Development and maintenance of expression of these region-specific genes is crucial for normal palate development. Numerous transcription factors and signaling pathways are now recognized as either anterior- (e.g., Msx1, Bmp4, Bmp2, Shh, Spry2, Fgf10, Fgf7, and Shox2) or posterior-specific (e.g., Meox2, Tbx22, and Barx1). Localized expression and function clearly highlight the importance of regional patterning and differentiation within the palate at the molecular level. Here, we review how these molecular pathways and networks regulate the anterior–posterior patterning and development of secondary palate. We hypothesize that the anterior palate acts as a signaling center in setting up development of the secondary palate.

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“…In addition to these endogenous patterning cues, cNCCs also receive external signals from surrounding cells and extracellular matrix, such as Fgf, BMP and Shh signals [10], [11], [12], [13], which are absolutely required for pharyngeal cartilage differentiation, segmentation, and cell survival. Recently, BMP signaling was shown to promote ventral arch development just after cNCC migration, however a later function for BMPs in craniofacial skeleton patterning was also shown [14].…”

Section: Introductionmentioning

confidence: 99%

RUNX3, EGR1 and SOX9B Form a Regulatory Cascade Required to Modulate BMP-Signaling during Cranial Cartilage Development in Zebrafish

et al. 2012

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The cartilaginous elements forming the pharyngeal arches of the zebrafish derive from cranial neural crest cells. Their proper differentiation and patterning are regulated by reciprocal interactions between neural crest cells and surrounding endodermal, ectodermal and mesodermal tissues. In this study, we show that the endodermal factors Runx3 and Sox9b form a regulatory cascade with Egr1 resulting in transcriptional repression of the fsta gene, encoding a BMP antagonist, in pharyngeal endoderm. Using a transgenic line expressing a dominant negative BMP receptor or a specific BMP inhibitor (dorsomorphin), we show that BMP signaling is indeed required around 30 hpf in the neural crest cells to allow cell differentiation and proper pharyngeal cartilage formation. Runx3, Egr1, Sox9b and BMP signaling are required for expression of runx2b, one of the key regulator of cranial cartilage maturation and bone formation. Finally, we show that egr1 depletion leads to increased expression of fsta and inhibition of BMP signaling in the pharyngeal region. In conclusion, we show that the successive induction of the transcription factors Runx3, Egr1 and Sox9b constitutes a regulatory cascade that controls expression of Follistatin A in pharyngeal endoderm, the latter modulating BMP signaling in developing cranial cartilage in zebrafish.

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Differential Shh, Bmp and Wnt gene expressions during craniofacial development in mice

Cited by 30 publications

References 48 publications

Studies with Wnt genes and nonsyndromic cleft lip and palate

Studies with Wnt genes and nonsyndromic cleft lip and palate

Molecular signaling along the anterior–posterior axis of early palate development

RUNX3, EGR1 and SOX9B Form a Regulatory Cascade Required to Modulate BMP-Signaling during Cranial Cartilage Development in Zebrafish

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