The organizer factors Chordin and Noggin are required for mouse forebrain development

Bachiller, Daniel; Klingensmith, John; Kemp, Caroline; Belo, José António; Anderson, Ryan M.; May, S. Randolph; McMahon, Jill A.; McMahon, Andrew P.; Harland, Richard M.; Rossant, Janet; Robertis, E. M. De

doi:10.1038/35001072

Cited by 496 publications

(363 citation statements)

References 30 publications

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“…During the development of many tissues, the action and local concentration of BMPs are controlled by specific antagonists and cell fates are specified by these molecules in a concentration-dependent manner (4,5,41). In vertebrate development, BMP4 is an important negative regulator of neural induction, whereas its antagonists Noggin and Chordin promote neural induction and are essential for patterning of the neural tube (5,16). As the BMP2/4 antagonists Chordin, Tsg, and Noggin are expressed in the thymus, it is possible that BMP2/4 signaling might work in a similar way to regulate T cell development.…”

Section: Discussionmentioning

confidence: 99%

“…Noggin was first identified as a dorsalizing factor in the Spemann organizer of Xenopus embryos (12), and mouse Noggin is required for patterning of the neural tube (13) and cartilage morphogenesis (14). Chordin also functions as a dorsalizing factor of the Xenopus Spemann organizer (15), and as a regulator of mammalian brain development (16). Tsg, which in Drosophila embryos specifies dorsal cell fate, has recently been shown to function as an extracellular BMP antagonist in vertebrates (17)(18)(19).…”

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confidence: 99%

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Bone Morphogenetic Protein 2/4 Signaling Regulates Early Thymocyte Differentiation

Hager-Theodorides

Outram

Shah

et al. 2002

The Journal of Immunology

112

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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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Bone Morphogenetic Protein 2/4 Signaling Regulates Early Thymocyte Differentiation

Hager-Theodorides

Outram

Shah

et al. 2002

The Journal of Immunology

112

131

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“…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: 91%

“…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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“…6G′ and data not shown). Chordin (Chrd), encoding a BMP-antagonist specifically expressed in the APS and in one of its derivatives, the notochord (Bachiller et al, 2000), was absent in N1ICD epi embryos (n=4; Fig. 6I,I′).…”

Section: Notch Activation Impairs Axial Mesoderm Formation and Perturmentioning

confidence: 99%

NOTCH activation interferes with cell fate specification in the gastrulating mouse embryo

et al. 2015

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NOTCH signalling is an evolutionarily conserved pathway involved in intercellular communication essential for cell fate choices during development. Although dispensable for early aspects of mouse development, canonical RBPJ-dependent NOTCH signalling has been shown to influence lineage commitment during embryonic stem cell (ESC) differentiation. NOTCH activation in ESCs promotes the acquisition of a neural fate, whereas its suppression favours their differentiation into cardiomyocytes. This suggests that NOTCH signalling is implicated in the acquisition of distinct embryonic fates at early stages of mammalian development. In order to investigate in vivo such a role for NOTCH signalling in shaping cell fate specification, we use genetic approaches to constitutively activate the NOTCH pathway in the mouse embryo. Early embryonic development, including the establishment of anterior-posterior polarity, is not perturbed by forced NOTCH activation. By contrast, widespread NOTCH activity in the epiblast triggers dramatic gastrulation defects. These are fully rescued in a RBPJ-deficient background. Epiblast-specific NOTCH activation induces acquisition of neurectoderm identity and disrupts the formation of specific mesodermal precursors including the derivatives of the anterior primitive streak, the mouse organiser. In addition, we show that forced NOTCH activation results in misregulation of NODAL signalling, a major determinant of early embryonic patterning. Our study reveals a previously unidentified role for canonical NOTCH signalling during mammalian gastrulation. It also exemplifies how in vivo studies can shed light on the mechanisms underlying cell fate specification during in vitro directed differentiation.

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The organizer factors Chordin and Noggin are required for mouse forebrain development

Cited by 496 publications

References 30 publications

Bone Morphogenetic Protein 2/4 Signaling Regulates Early Thymocyte Differentiation

Bone Morphogenetic Protein 2/4 Signaling Regulates Early Thymocyte Differentiation

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

NOTCH activation interferes with cell fate specification in the gastrulating mouse embryo

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