Developmental Signals - Bone Morphogenetic Protein: Difference between revisions

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Molecular paracrine interactions involving BMP signaling<ref><pubmed>24711992</pubmed>| [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3966335 PMC3966335] | [http://www.hindawi.com/journals/bmri/2014/213570 Biomed Res Int.]</ref>
Molecular paracrine interactions involving BMP15 signaling<ref><pubmed>24711992</pubmed>| [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3966335 PMC3966335] | [http://www.hindawi.com/journals/bmri/2014/213570 Biomed Res Int.]</ref>


==Signaling Pathway==
==Signaling Pathway==

Revision as of 09:36, 16 November 2014

Embryology - 28 Mar 2024    Facebook link Pinterest link Twitter link  Expand to Translate  
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Introduction

Belongs to the transforming growth factor-beta (TGFB) superfamily.


TGFB family members: TGFB1, TGFB, TGFB3, bone morphogenetic proteins Bmp-2A, Bmp-2B, Bmp-3, and Bmp-6. mullerian inhibitory substance.

Mouse Bmp4 expression face 01.jpg

Mouse Bmp4 expression face.[1]


BMP Mouse Links: Face and limb E9.5-13.5 | Face E9.5-13.5 | Body E11.0 | Body E11.5 | BMP | Mouse Development

Growth Differentiation Factor-6 (Gdf6) is a member of the Bone Morphogenetic Protein (BMP) family of secreted signaling molecules.

Factor Links: AMH | hCG | BMP | sonic hedgehog | bHLH | HOX | FGF | FOX | Hippo | LIM | Nanog | NGF | Nodal | Notch | PAX | retinoic acid | SIX | Slit2/Robo1 | SOX | TBX | TGF-beta | VEGF | WNT | Category:Molecular

Some Recent Findings

  • Construction of a vertebrate embryo from two opposing morphogen gradients[2] "Here, we show that opposing gradients of bone morphogenetic protein (BMP) and Nodal, two transforming growth factor family members that act as morphogens, are sufficient to induce molecular and cellular mechanisms required to organize, in vivo or in vitro, uncommitted cells of the zebrafish blastula animal pole into a well-developed embryo." Zebrafish Development
  • Developmental stalling and organ-autonomous regulation of morphogenesis[3] "Timing of organ development during embryogenesis is coordinated such that at birth, organ and fetal size and maturity are appropriately proportioned. The extent to which local developmental timers are integrated with each other and with the signaling interactions that regulate morphogenesis to achieve this end is not understood. Using the absolute requirement for a signaling pathway activity (bone morphogenetic protein, BMP) during a critical stage of tooth development, we show that suboptimal levels of BMP signaling do not lead to abnormal morphogenesis, as suggested by mutants affecting BMP signaling, but to a 24-h stalling of the intrinsic developmental clock of the tooth. During this time, BMP levels accumulate to reach critical levels whereupon tooth development restarts, accelerates to catch up with development of the rest of the embryo and completes normal morphogenesis. This suggests that individual organs can autonomously control their developmental timing to adjust their stage of development to that of other organs. We also find that although BMP signaling is critical for the bud-to-cap transition in all teeth, levels of BMP signaling are regulated differently in multicusped teeth. We identify an interaction between two homeodomain transcription factors, Barx1 and Msx1, which is responsible for setting critical levels of BMP activity in multicusped teeth and provides evidence that correlates the levels of Barx1 transcriptional activity with cuspal complexity. This study highlights the importance of absolute levels of signaling activity for development and illustrates remarkable self-regulation in organogenesis that ensures coordination of developmental processes such that timing is subordinate to developmental structure."
More recent papers
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Search term: Bone Morphogenetic Protein

<pubmed limit=5>Bone Morphogenetic Protein</pubmed>

Structure

Gene

Function

Mouse Bmp4 expression limb and face 01.jpg

Mouse Bmp4 expression limb and face.[4]

Mouse face Bmp4 icon.jpg
 ‎‎Mouse Face Bmp4
Page | Play

Oocyte Development

Ovarian follicle molecular interactions

Molecular paracrine interactions involving BMP15 signaling[5]

Signaling Pathway

Identified BMP modulators:[6] Noggin, Chordin, Chordin-like 1, Chordin-like 2, Twisted gastrulation, Dan, BMPER, Sost, Sostdc1, Follistatin, Follistatin-like 1, Follistatin-like 5 and Tolloid.

Receptor

Intracellular Signaling

SNW-domain containing protein 1

(SNW1, SKI-INTERACTING PROTEIN; SKIIP)

A protein that interacts with nuclear receptors and enhances ligand-activated transcription, also called a nuclear receptor co-activator.


Regulator of Spatial BMP Activity, Neural Plate Border Formation, and Neural Crest Specification in Vertebrate Embryos[7]

"Bone morphogenetic protein (BMP) gradients provide positional information to direct cell fate specification, such as patterning of the vertebrate ectoderm into neural, neural crest, and epidermal tissues, with precise borders segregating these domains. However, little is known about how BMP activity is regulated spatially and temporally during vertebrate development to contribute to embryonic patterning, and more specifically to neural crest formation. Through a large-scale in vivo functional screen in Xenopus for neural crest fate, we identified an essential regulator of BMP activity, SNW1. SNW1 is a nuclear protein known to regulate gene expression. Using antisense morpholinos to deplete SNW1 protein in both Xenopus and zebrafish embryos, we demonstrate that dorsally expressed SNW1 is required for neural crest specification, and this is independent of mesoderm formation and gastrulation morphogenetic movements. By exploiting a combination of immunostaining for phosphorylated Smad1 in Xenopus embryos and a BMP-dependent reporter transgenic zebrafish line, we show that SNW1 regulates a specific domain of BMP activity in the dorsal ectoderm at the neural plate border at post-gastrula stages. We use double in situ hybridizations and immunofluorescence to show how this domain of BMP activity is spatially positioned relative to the neural crest domain and that of SNW1 expression. Further in vivo and in vitro assays using cell culture and tissue explants allow us to conclude that SNW1 acts upstream of the BMP receptors. Finally, we show that the requirement of SNW1 for neural crest specification is through its ability to regulate BMP activity, as we demonstrate that targeted overexpression of BMP to the neural plate border is sufficient to restore neural crest formation in Xenopus SNW1 morphants. We conclude that through its ability to regulate a specific domain of BMP activity in the vertebrate embryo, SNW1 is a critical regulator of neural plate border formation and thus neural crest specification."

Additional Images

OMIM

About OMIM "Online Mendelian Inheritance in Man OMIM is a comprehensive, authoritative, and timely compendium of human genes and genetic phenotypes. The full-text, referenced overviews in OMIM contain information on all known mendelian disorders and over 12,000 genes. OMIM focuses on the relationship between phenotype and genotype. It is updated daily, and the entries contain copious links to other genetics resources." OMIM


References

  1. PLoS One
  2. <pubmed>24700857</pubmed>
  3. <pubmed>22084104</pubmed>
  4. PLoS One
  5. <pubmed>24711992</pubmed>| PMC3966335 | Biomed Res Int.
  6. <pubmed>23573253</pubmed>
  7. <pubmed>21358802</pubmed>

Reviews

<pubmed>24174749</pubmed> <pubmed>22327483</pubmed> <pubmed>17029022</pubmed> <pubmed>15621726</pubmed>

Articles

<pubmed></pubmed> <pubmed></pubmed> <pubmed>23055827</pubmed> <pubmed>22693607</pubmed>

Online Textbooks


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Cite this page: Hill, M.A. (2024, March 28) Embryology Developmental Signals - Bone Morphogenetic Protein. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Developmental_Signals_-_Bone_Morphogenetic_Protein

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© Dr Mark Hill 2024, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G