TGFβ-mediated FGF signaling is crucial for regulating cranial neural crest cell proliferation during frontal bone development

Sasaki, Taro; Ito, Yoshihiro; Bringas, Pablo; Chou, Stanley S.; Urata, Mark M.; Slavkin, Harold C.; Chai, Yang

doi:10.1242/dev.02200

Cited by 84 publications

(83 citation statements)

References 46 publications

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“…Hematoxylin and eosin staining and BrdU staining were performed as described previously (13,52). Immunohistochemical staining was performed as described previously (53).…”

Section: Discussionmentioning

confidence: 99%

Modulation of noncanonical TGF-β signaling prevents cleft palate in Tgfbr2 mutant mice

et al. 2012

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Patients with mutations in either TGF-β receptor type I (TGFBR1) or TGF-β receptor type II (TGFBR2), such as those with Loeys-Dietz syndrome, have craniofacial defects and signs of elevated TGF-β signaling. Similarly, mutations in TGF-β receptor gene family members cause craniofacial deformities, such as cleft palate, in mice. However, it is unknown whether TGF-β ligands are able to elicit signals in Tgfbr2 mutant mice. Here, we show that loss of Tgfbr2 in mouse cranial neural crest cells results in elevated expression of TGF-β2 and TGF-β receptor type III (TβRIII); activation of a TβRI/TβRIII-mediated, SMAD-independent, TRAF6/TAK1/p38 signaling pathway; and defective cell proliferation in the palatal mesenchyme. Strikingly, Tgfb2, Tgfbr1 (also known as Alk5), or Tak1 haploinsufficiency disrupted TβRI/TβRIII-mediated signaling and rescued craniofacial deformities in Tgfbr2 mutant mice, indicating that activation of this noncanonical TGF-β signaling pathway was responsible for craniofacial malformations in Tgfbr2 mutant mice. Thus, modulation of TGF-β signaling may be beneficial for the prevention of congenital craniofacial birth defects.

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“…Hematoxylin and eosin staining and BrdU staining were performed as described previously (13,52). Immunohistochemical staining was performed as described previously (53).…”

Section: Discussionmentioning

confidence: 99%

Modulation of noncanonical TGF-β signaling prevents cleft palate in Tgfbr2 mutant mice

et al. 2012

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“…Combined functions of TGFβ and FGF signaling that manifest in synergism or epistasis of the two signaling cascades have been reported in a number of developmental and disease processes, including survival of dopaminergic neurons (Roussa et al, 2004), development of lens cataracts (Cerra et al, 2003), chondrocyte proliferation (Mukherjee et al, 2005) and the development of calvarial bones (Sasaki et al, 2006). As both FGF and TGFβ signaling have now been shown to induce early tendon markers, it will be important to establish in future studies the relationships between these signaling cascades in tendon induction.…”

Section: ;Tgfb3mentioning

confidence: 99%

Recruitment and maintenance of tendon progenitors by TGFβ signaling are essential for tendon formation

et al. 2009

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Tendons and ligaments mediate the attachment of muscle to bone and of bone to bone to provide connectivity and structural integrity in the musculoskeletal system. We show that TGFβ signaling plays a major role in the formation of these tissues. TGFβ signaling is a potent inducer of the tendon progenitor (TNP) marker scleraxis both in organ culture and in cultured cells, and disruption of TGFβ signaling in Tgfb2-/-double mutant embryos or through inactivation of the type II TGFβ receptor (TGFBR2; also known as TβRII) results in the loss of most tendons and ligaments in the limbs, trunk, tail and head. The induction of scleraxis-expressing TNPs is not affected in mutant embryos and the tendon phenotype is first manifested at E12.5, a developmental stage in which TNPs are positioned between the differentiating muscles and cartilage, and in which Tgfb2 or Tgfb3 is expressed both in TNPs and in the differentiating muscles and cartilage. TGFβ signaling is thus essential for maintenance of TNPs, and we propose that it also mediates the recruitment of new tendon cells by differentiating muscles and cartilage to establish the connections between tendon primordia and their respective musculoskeletal counterparts, leading to the formation of an interconnected and functionally integrated musculoskeletal system.

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“…3D). The dura mater that underlies the frontal and parietal bones is also neural crest derived Ito et al, 2003;Sasaki et al, 2006). The coronal and sagittal sutures are of mesoderm origin (Morriss-Kay and Wilkie, 2005).…”

Section: Skull Development and Tissue Boundarymentioning

confidence: 99%

Recent advances in craniofacial morphogenesis

Chai

Maxson

2006

Developmental Dynamics

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Craniofacial malformations are involved in three fourths of all congenital birth defects in humans, affecting the development of head, face, or neck. Tremendous progress in the study of craniofacial development has been made that places this field at the forefront of biomedical research. A concerted effort among evolutionary and developmental biologists, human geneticists, and tissue engineers has revealed important information on the molecular mechanisms that are crucial for the patterning and formation of craniofacial structures. Here, we highlight recent advances in our understanding of evo-devo as it relates to craniofacial morphogenesis, fate determination of cranial neural crest cells, and specific signaling pathways in regulating tissue-tissue interactions during patterning of craniofacial apparatus and the morphogenesis of tooth, mandible, and palate. Together, these findings will be beneficial for the understanding, treatment, and prevention of human congenital malformations and establish the foundation for craniofacial tissue regeneration. Developmental Dynamics 235:2353-2375, 2006.

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TGFβ-mediated FGF signaling is crucial for regulating cranial neural crest cell proliferation during frontal bone development

Cited by 84 publications

References 46 publications

Modulation of noncanonical TGF-β signaling prevents cleft palate in Tgfbr2 mutant mice

Modulation of noncanonical TGF-β signaling prevents cleft palate in Tgfbr2 mutant mice

Recruitment and maintenance of tendon progenitors by TGFβ signaling are essential for tendon formation

Recent advances in craniofacial morphogenesis

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