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| ==Introduction== | | ==Introduction== |
| | | [[File:Notch structure cartoon.jpg|thumb|300px|alt=Notch structure cartoon|Notch structure cartoon<ref><pubmed>19255248</pubmed></ref>]] |
| The notch proteins were first identified in drosophila development and have since been identified as regulators of cell fate decisions during development. These are a family of cell surface transmembrane receptors that pass once through the plasma membrane. | | The notch proteins were first identified in drosophila development and have since been identified as regulators of cell fate decisions during development. These are a family of cell surface transmembrane receptors that pass once through the plasma membrane. |
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Revision as of 20:54, 4 February 2015
Introduction
Notch structure cartoon
[1]The notch proteins were first identified in drosophila development and have since been identified as regulators of cell fate decisions during development. These are a family of cell surface transmembrane receptors that pass once through the plasma membrane.
- Notch Links: Notch structure cartoon | Notch signaling pathway cartoon | Notch and signaling pathway cartoon | Developmental Signals - Notch | Molecular Factors
Some Recent Findings
Mouse somitogenesis genes
[2]
- Notch regulation of myogenic versus endothelial fates of cells that migrate from the somite to the limb[3] "Multipotent Pax3-positive (Pax3(+)) cells in the somites give rise to skeletal muscle and to cells of the vasculature. We had previously proposed that this cell-fate choice depends on the equilibrium between Pax3 and Foxc2 expression. In this study, we report that the Notch pathway promotes vascular versus skeletal muscle cell fates. ...We now demonstrate that in addition to the inhibitory role of Notch signaling on skeletal muscle cell differentiation, the Notch pathway affects the Pax3:Foxc2 balance and promotes the endothelial versus myogenic cell fate, before migration to the limb, in multipotent Pax3(+) cells in the somite of the mouse embryo." Limb Development | Muscle Development
- The precise timeline of transcriptional regulation reveals causation in mouse somitogenesis network[2] "In vertebrate development, the segmental pattern of the body axis is established as somites, masses of mesoderm distributed along the two sides of the neural tube, are formed sequentially in the anterior-posterior axis. This mechanism depends on waves of gene expression associated with the Notch, Fgf and Wnt pathways."
- Role of p63 and the Notch pathway in cochlea development and sensorineural deafness[4] "The ectodermal dysplasias are a group of inherited autosomal dominant syndromes associated with heterozygous mutations in the Tumor Protein p63 (TRP63) gene. Here we show that, in addition to their epidermal pathology, a proportion of these patients have distinct levels of deafness. ...these data demonstrate that TAp63, acting via the Notch pathway, is crucial for the development of the organ of Corti, providing a molecular explanation for the sensorineural deafness in ectodermal dysplasia patients with TRP63 mutations." Sensory - Hearing and Balance Development
- Notch signaling regulates late-stage epidermal differentiation and maintains postnatal hair cycle homeostasis [5] "Notch signaling involves ligand-receptor interactions through direct cell-cell contact. Multiple Notch receptors and ligands are expressed in the epidermis and hair follicles during embryonic development and the adult stage. Although Notch signaling plays an important role in regulating differentiation of the epidermis and hair follicles, it remains unclear how Notch signaling participates in late-stage epidermal differentiation and postnatal hair cycle homeostasis. ...our data reveal a role for Notch signaling in regulating late-stage epidermal differentiation. Notch signaling is required for postnatal hair cycle homeostasis by maintaining proper proliferation and differentiation of hair follicle stem cells."
- Notch pathway regulation of chondrocyte differentiation and proliferation during appendicular and axial skeleton development [6] "The role of Notch signaling in cartilage differentiation and maturation in vivo was examined. Conditional Notch pathway gain and loss of function was achieved using a Cre/loxP approach to manipulate Notch signaling in cartilage precursors and chondrocytes of the developing mouse embryo. Conditional overexpression of activated Notch intracellular domain (NICD) in the chondrocyte lineage results in skeletal malformations with decreased cartilage precursor proliferation and inhibited hypertrophic chondrocyte differentiation. Likewise, expression of NICD in cartilage precursors inhibits sclerotome differentiation, resulting in severe axial skeleton abnormalities. Furthermore, conditional loss of Notch signaling via RBP-J gene deletion in the chondrocyte lineage results in increased chondrocyte proliferation and skeletal malformations consistent with the observed increase in hypertrophic chondrocytes. In addition, the Notch pathway inhibits expression of Sox9 and its target genes required for normal chondrogenic cell proliferation and differentiation. Together, our results demonstrate that appropriate Notch pathway signaling is essential for proper chondrocyte progenitor proliferation and for the normal progression of hypertrophic chondrocyte differentiation into bone in the developing appendicular and axial skeletal elements."
- Notch signalling in the paraxial mesoderm is most sensitive to reduced Pofut1 levels during early mouse development[7] "Notch-dependent processes apparently differ with respect to their requirement for levels of POFUT1. Normal Lfng expression and anterior-posterior somite patterning is highly sensitive to reduced POFUT1 levels in early mammalian embryos, whereas other early Notch-dependent processes such as establishment of left-right asymmetry or neurogenesis are not. Thus, it appears that in the presomitic mesoderm (PSM) Notch signalling is particularly sensitive to POFUT1 levels. Reduced POFUT1 levels might affect Notch trafficking or overall O-fucosylation. Alternatively, reduced O-fucosylation might preferentially affect sites that are substrates for LFNG and thus important for somite formation and patterning."
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| More recent papers
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More? References | Discussion Page | Journal Searches | 2019 References | 2020 References
Search term: Notch
<pubmed limit=5>Notch</pubmed>
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Notch Receptors
NOTCH1
NOTCH2
NOTCH3
- Notch3 activation retains mammary luminal cell in a nonproliferative state.[8]
NOTCH4
Notch Ligands
Functions
Developmental patterning signal.
Mesoderm Development
Cartilage Development
Muscle Regeneration
Notch signalling in muscle regeneration[9]
Hypothalamus Development
Hypothalamus Development Gene Interaction Model[10]
- Links: Hypothalamus Development
References
- ↑ <pubmed>19255248</pubmed>
- ↑ 2.0 2.1 <pubmed>24304493</pubmed>| BMC Dev Biol.
- ↑ <pubmed>24927569</pubmed>
- ↑ <pubmed>20513039</pubmed>
- ↑ <pubmed>19590010</pubmed>
- ↑ <pubmed>19590010</pubmed>
- ↑ <pubmed>19161597</pubmed>
- ↑ <pubmed>24100291</pubmed>
- ↑ <pubmed>24472470</pubmed>| BMC Dev Biol.
- ↑ 24360028<pubmed>24360028</pubmed>| Neural Dev.
Reviews
<pubmed></pubmed>
<pubmed></pubmed>
<pubmed></pubmed>
<pubmed>23165243</pubmed>
<pubmed> 22399351</pubmed>
<pubmed>22397947</pubmed>
<pubmed>21828089</pubmed>
Search Pubmed
Search Bookshelf Notch
Search Pubmed Now: Notch Signaling
External Links
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Cite this page: Hill, M.A. (2024, April 18) Embryology Developmental Signals - Notch. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Developmental_Signals_-_Notch
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- © Dr Mark Hill 2024, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G
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