Noggin, Cartilage Morphogenesis, and Joint Formation in the Mammalian Skeleton

Brunet, Lisa J.; McMahon, Jill A.; McMahon, Andrew P.; Harland, Richard M.

doi:10.1126/science.280.5368.1455

Cited by 768 publications

(605 citation statements)

References 16 publications

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“…These syndromes were shown to be caused by mutations in the BMP antagonist NOG-GIN (NOG; Gong et al, 1999;Dixon et al, 2001;Takahashi et al, 2001;Brown et al, 2002) indicating that inhibition of BMP signaling is pivotal for the process of joint formation. Corroborating this, disruption of the mouse Noggin gene results in enlarged condensations and joint fusions (Brunet et al, 1998). Of interest, a certain subset of mutations in GDF5 were also shown to be associated with joint fusions (Seemann et al, 2005;Dawson et al, 2006;Wang et al, 2006;Yang et al, 2008;).…”

Section: Segmentation Of the Digitsmentioning

confidence: 91%

Mechanisms of digit formation: Human malformation syndromes tell the story

Stricker

Mundlos

2011

Developmental Dynamics

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Identifying the genetic basis of human limb malformation disorders has been instrumental in improving our understanding of limb development. Abnormalities of the hands and/or feet include defects affecting patterning, establishment, elongation, and segmentation of cartilaginous condensations, as well as growth of the individual skeletal elements. While the phenotype of such malformations is highly diverse, the mutations identified to date cluster in genes implicated in a limited number of molecular pathways, namely hedgehog, Wnt, and bone morphogenetic protein. The latter pathway appears to function as a key molecular network regulating different phases of digit and joint development. Studies in animal models not only extended our insight into the pathogenesis of these conditions, but have also contributed to our understanding of the in vivo functions and interactions of these key players. This review is aimed at integrating the current understanding of human digit malformations into the increasing knowledge of the molecular mechanisms of digit development. Developmental Dynamics 240:990-1004,

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Section: Segmentation Of the Digitsmentioning

confidence: 91%

Mechanisms of digit formation: Human malformation syndromes tell the story

Stricker

Mundlos

2011

Developmental Dynamics

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“…However, the severe chondrogenesis defects of Nog Ϫ/Ϫ mutants (Brunet et al, 1998) obscure phenotypes specific to the NCC-derived skeleton, and Chrd Ϫ/Ϫ ;Nog Ϫ/Ϫ mutants die before skeletogenesis (Bachiller et al, 2000). We, therefore, focused on craniofacial defects in Chrd Ϫ/Ϫ ; Nog ϩ/Ϫ mutants.…”

Section: Depletion Of Migratory Neural Crest Cells Inmentioning

confidence: 99%

Endogenous bone morphogenetic protein antagonists regulate mammalian neural crest generation and survival

Anderson

Stottmann

Choi

et al. 2006

Developmental Dynamics

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We demonstrate here that Chordin and Noggin function as bone morphogenetic protein (BMP) antagonists in vivo to promote mammalian neural crest development. Using Chrd and Nog single and compound mutants, we find that Noggin has a major role in promoting neural crest formation, in which Chordin is partially redundant. BMP signaling is increased in dorsal tissues lacking Noggin and is further increased when Chordin is also absent. The early neural crest domain is expanded with decreased BMP antagonism in vivo. Noggin and Chordin also regulate subsequent neural crest cell emigration from the neural tube. However, reduced levels of these BMP antagonists ultimately result in perturbation of neural crest cell derived peripheral nervous system and craniofacial skeletal elements. Such defects reflect, at least in part, a function to limit apoptosis in neural crest cells. Noggin and Chordin, therefore, function together to regulate both the generation and survival of neural crest cells in mammalian development. Developmental Dynamics 235:2507-2520, 2006.

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“…Embryonic chicken chondrocytes expressing constitutively active BMP type I receptors had increased Ihh expression, which was not blocked by PTHrP, implying that BMPs stimulation of Ihh is independent of the effect of BMPs on chondrocyte hypertrophy. Similarly, BMP2-treated embryonic limb explants also had increased Ihh expression, which was blocked by Noggin [Brunet et al, 1998]. …”

Section: Bone Morphogenic Proteins As Mediators Of Ihh Regulationmentioning

confidence: 99%

Indian hedgehog: Its roles and regulation in endochondral bone development

Lai

Mitchell

2005

J of Cellular Biochemistry

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Normal endochondral bone development requires the coordination of chondrocyte proliferation and differentiation. Indian hedgehog (Ihh) is a morphogen produced by chondrocytes in the early stage of terminal differentiation and plays several key roles in this process. Ihh regulates growth of adjacent proliferative chondrocytes and can also regulate the rate of differentiation of chondrocytes indirectly through its stimulation of parathyroid hormonerelated protein (PTHrP). In this review, we focus on recent studies that have identified new functions of Ihh and how Ihh itself is being regulated.

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Noggin, Cartilage Morphogenesis, and Joint Formation in the Mammalian Skeleton

Cited by 768 publications

References 16 publications

Mechanisms of digit formation: Human malformation syndromes tell the story

Mechanisms of digit formation: Human malformation syndromes tell the story

Endogenous bone morphogenetic protein antagonists regulate mammalian neural crest generation and survival

Indian hedgehog: Its roles and regulation in endochondral bone development

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