A truncated bone morphogenetic protein 4 receptor alters the fate of ventral mesoderm to dorsal mesoderm: roles of animal pole tissue in the development of ventral mesoderm.

Maéno, Mitsugu; Ong, Rosa Chua; Suzuki, Atsushi; Ueno, Naoto; Kung, Hsiang‐Fu

doi:10.1073/pnas.91.22.10260

Cited by 150 publications

(74 citation statements)

References 28 publications

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“…To elucidate the involvement of BMPR-IA in the BMP-2 signaling in C2C12 cells, a kinase domain-truncated BMPR-IA was constructed and stably transfected into C2C12 cells. This truncated BMPR-IA acts as a dominant negative receptor for BMP-4 signaling in the Xenopus embryo (23,34,35). When the kinase domain-truncated BMPR-IA was overexpressed in C2C12 myoblasts, they differentiated into MHC-positive myotubes but not into osteoblastlike ALP-positive cells, even in the presence of BMP-2.…”

Section: Discussionmentioning

confidence: 99%

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A Kinase Domain-truncated Type I Receptor Blocks Bone Morphogenetic Protein-2-induced Signal Transduction in C2C12 Myoblasts

Namiki

Akiyama

Katagiri

et al. 1997

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 99%

“…A kinase domain-truncated BMPR-IA abolished the ventralizing activity of BMP-4 in a dominant negative manner in the Xenopus embryo (23,34,35). We therefore examined whether a dominant negative BMP type I receptor could inhibit the BMP-2-induced signalings in myoblasts.…”

mentioning

confidence: 99%

A Kinase Domain-truncated Type I Receptor Blocks Bone Morphogenetic Protein-2-induced Signal Transduction in C2C12 Myoblasts

Namiki

Akiyama

Katagiri

et al. 1997

Journal of Biological Chemistry

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“…In addition to a modulation of Wnt signals, differentiation of lateral plate mesoderm into either an anterior (i.e., heart) or posterior (i.e., blood) cell fate requires concomitant BMP signaling (Dale et al 1992;Jones et al 1992;Fainsod et al 1994;Graff et al 1994;Maeno et al 1994;Suzuki et al 1994;Andreé et al 1998;Schlange et al 2000), which is present only in the lateral (ventral) domains of the embryo. Thus, mesoderm located in regions of the gastrula stage embryo that are exposed to low levels of Wnt signaling and high levels of BMP signals develop into cardiac tissue (illustrated in Fig.…”

Section: Wnt Inhibition Promotes Heart Muscle Formation From Posteriomentioning

confidence: 99%

Inhibition of Wnt activity induces heart formation from posterior mesoderm

Marvin¹,

Rocco²,

Gardiner³

et al. 2001

Genes Dev.

541

459

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In the chick, heart mesoderm is induced by signals from the anterior endoderm. Although BMP-2 is expressed in the anterior endoderm, BMP activity is necessary but not sufficient for heart formation. Previous work from our lab has suggested that one or more additional factors from anterior endoderm are required. Crescent is a Frizzled-related protein that inhibits Wnt-8c and is expressed in anterior endoderm during gastrulation. At the same stages, expression of Wnt-3a and Wnt-8c is restricted to the primitive streak and posterior lateral plate, and is absent from the anterior region where crescent is expressed. Posterior lateral plate mesoderm normally forms blood, but coculture of this tissue with anterior endoderm or infection with RCAS-crescent induces formation of beating heart muscle and represses formation of blood. Dkk-1, a Wnt inhibitor of a different protein family, similarly induces heart-specific gene expression in posterior lateral plate mesoderm. Furthermore, we have found that ectopic Wnt signals can repress heart formation from anterior mesoderm in vitro and in vivo and that forced expression of either Wnt-3a or Wnt-8c can promote development of primitive erythrocytes from the precardiac region. We conclude that inhibition of Wnt signaling promotes heart formation in the anterior lateral mesoderm, whereas active Wnt signaling in the posterior lateral mesoderm promotes blood development. We propose a model in which two orthogonal gradients, one of Wnt activity along the anterior-posterior axis and the other of BMP signals along the dorsal-ventral axis, intersect in the heart-forming region to induce cardiogenesis in a region of high BMP and low Wnt activity.

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“…Thus, we are now examining the expression pattern of the genes encoding the above-mentioned secretory proteins and planning to examine the effect of these secretory proteins on the flounder-specific adult pigment pattern. Because it has been reported that the signaling by these secretory proteins is involved in embryonic dorsoventral axis formation (Smith et al, 1993;Graff et al, 1994;Maeno et al, 1994;Suzuki et al, 1994;Funayama et al, 1995;He et al, 1995;Schneider et al, 1996;Sokol, 1996;Sumoy et al, 1999;Cho et al, 2006), we are very interested in whether these proteins may relate to the conversion from left-right axis to dorsalventral axis in flatfish during the process of metamorphosis.…”

Section: Japanese Flounder Adulttype Pigment Cells Are Derived From Dmentioning

confidence: 99%

Origin of adult‐type pigment cells forming the asymmetric pigment pattern, in Japanese flounder (Paralichthys olivaceus)

Yamada

Okauchi

Araki

2010

Developmental Dynamics

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The flatfish-specific asymmetric pigment pattern depends on the asymmetric appearance of adult-type pigment cells after the late metamorphic stages. To understand the mechanism enabling the formation of this asymmetric pattern, we investigated the behavior of pigment cell latent precursors in postembryonic Japanese flounder, Paralichthys olivaceus, by analysis of the expression patterns of pigment lineage markers (colony stimulating factor 1 receptor, dopachrome tautomerase, kit) and the DiI (DiO) labeling test for latent precursors. We found that, throughout the larval stages, pigment cell latent precursors were predominantly localized along the dorsal and ventral margins of the flank symmetrically and migrated continuously from these regions to the lateral sides symmetrically, and after late metamorphic stages these precursors differentiated into adult-type pigment cells on the lateral side asymmetrically. We conclude that adult-type pigment cells that form the asymmetric pigment pattern are continuously derived from the dorsal and ventral margins of the flank during larval development. Developmental Dynamics 239:3147-3162,

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A truncated bone morphogenetic protein 4 receptor alters the fate of ventral mesoderm to dorsal mesoderm: roles of animal pole tissue in the development of ventral mesoderm.

Abstract: The biological effects of endogenous bone morphogenetic protein 4 (BMP-4), a member of the transforming growth factor 13 family, on embryonic development of Xenopus laevis were investigated by using a functionally defective mutant of the BMP-4 receptor (AmTFR11)

Cited by 150 publications

References 28 publications

A Kinase Domain-truncated Type I Receptor Blocks Bone Morphogenetic Protein-2-induced Signal Transduction in C2C12 Myoblasts

A Kinase Domain-truncated Type I Receptor Blocks Bone Morphogenetic Protein-2-induced Signal Transduction in C2C12 Myoblasts

Inhibition of Wnt activity induces heart formation from posterior mesoderm

Origin of adult‐type pigment cells forming the asymmetric pigment pattern, in Japanese flounder (Paralichthys olivaceus)

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