Spatiotemporal expression patterns of mammalian chordin during postgastrulation embryogenesis and in postnatal brain

Scott, Ian C.; Steiglitz, Barry M.; Clark, Timothy G.; Pappano, William N.; Greenspan, Daniel S.

doi:10.1002/(sici)1097-0177(200004)217:4<449::aid-dvdy12>3.0.co;2-8

Cited by 51 publications

(44 citation statements)

References 39 publications

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“…3A-C; McMahon et al, 1998). Meanwhile, Chordin is expressed at a very low, fairly even level throughout the neural plate and paraxial mesoderm, as indicated by section and whole-mount in situ hybridization and confirmed by reverse transcriptase-polymerase chain reaction of microdissected tissues (data not shown; Scott et al, 2000). Together, these considerations suggest that both of these proteins may regulate BMP signaling in the dorsal neural folds during neural crest generation.…”

Section: Chordin and Noggin Antagonize Bmp Signaling In The Dorsal Nementioning

confidence: 84%

“…During organogenesis stages, Chordin is broadly expressed at very low levels (Scott et al, 2000; data not shown), with higher levels in the notochord and dorsal foregut endoderm (Bachiller et al, 2000;Stottmann et al, 2001). Besides the dorsal neural tube, Noggin is expressed in the notochord, dorsal foregut endoderm, and anterior neural ridge; in addition, Noggin appears to be expressed in some migrating cranial NCCs in mouse embryos Stottmann et al, 2001;Anderson et al, 2002).…”

Section: Bmp Antagonism Is Required For Survival Of Migratory Nccsmentioning

confidence: 93%

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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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Section: Chordin and Noggin Antagonize Bmp Signaling In The Dorsal Nementioning

confidence: 84%

Section: Bmp Antagonism Is Required For Survival Of Migratory Nccsmentioning

confidence: 93%

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

Anderson

Stottmann

Choi

et al. 2006

Developmental Dynamics

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“…However, whether Tsg exerts its regulating function in cartilage through the interaction with chordin remains questionable, because chordin is absent from all fetal bovine growth plate chondrocyte populations except for resting chondrocytes (51). In situ hybridization studies of the developing mouse skeleton showed the absence of chordin from cartilage proper (52,53). Thus, at least in the regulation of BMP activity by Tsg in cartilage, other modulator proteins might be at work.…”

Section: Discussionmentioning

confidence: 99%

von Willebrand Factor Type C Domain-containing Proteins Regulate Bone Morphogenetic Protein Signaling through Different Recognition Mechanisms

Zhang

Huang

Qiu

et al. 2007

Journal of Biological Chemistry

104

130

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“…Mouse Tsg is expressed during lymphocyte development (22), and Chordin (23), BMP4 (24), and the Smad-interacting transcription factor Schnurri-2 (25) are expressed in the mouse thymus, suggesting that BMP signaling may play a role in thymocyte development.…”

mentioning

confidence: 99%

Bone Morphogenetic Protein 2/4 Signaling Regulates Early Thymocyte Differentiation

Hager-Theodorides

Outram

Shah

et al. 2002

The Journal of Immunology

111

131

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Bone morphogenetic protein (BMP)2 and BMP4 are involved in the development of many tissues. In this study, we show that BMP2/4 signaling is involved in thymocyte development. Our data suggest that termination of BMP2/4 signaling is necessary for differentiation of CD44+CD25−CD4−CD8− double negative (DN) cells along the T cell lineage. BMP2 and BMP4 are produced by the thymic stroma and the requisite BMP receptor molecules (BMPR-1A, BMPR-1B, BMPR-II), and signal transduction molecules (Smad-1, -5, -8, and -4) are expressed by DN thymocytes. BMP4 inhibits thymocyte proliferation, enhances thymocyte survival, and arrests thymocyte differentiation at the CD44+CD25− DN stage, before T cell lineage commitment. Neutralization of endogenous BMP2 and BMP4 by treatment with the antagonist Noggin promotes and accelerates thymocyte differentiation, increasing the expression of CD2 and the proportion of CD44−CD25− DN cells and CD4+CD8+ double-positive cells. Our study suggests that the BMP2/4 pathway may function in thymic homeostasis by regulating T cell lineage commitment and differentiation.

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Spatiotemporal expression patterns of mammalian chordin during postgastrulation embryogenesis and in postnatal brain

Cited by 51 publications

References 39 publications

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

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

von Willebrand Factor Type C Domain-containing Proteins Regulate Bone Morphogenetic Protein Signaling through Different Recognition Mechanisms

Bone Morphogenetic Protein 2/4 Signaling Regulates Early Thymocyte Differentiation

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