Talk:Developmental Signals - Notch

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On this website the Discussion Tab or "talk pages" for a topic has been used for several purposes: References - recent and historic that relates to the topic Additional topic information - currently prepared in draft format Links - to related webpages Topic page - an edit history as used on other Wiki sites Lecture/Practical - student feedback Student Projects - online project discussions. Links: Pubmed Most Recent | Reference Tutorial | Journal Searches Glossary Links Glossary: A | B | C | D | E | F | G | H | I | J | K | L | M | N | O | P | Q | R | S | T | U | V | W | X | Y | Z | Numbers | Symbols | Term Link Cite this page: Hill, M.A. (2024, May 27) Embryology Developmental Signals - Notch. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Developmental_Signals_-_Notch

2011

Notch signaling regulates late-stage epidermal differentiation and maintains postnatal hair cycle homeostasis

PLoS One. 2011 Jan 18;6(1):e15842.

Lin HY, Kao CH, Lin KM, Kaartinen V, Yang LT. Institute of Cellular and System Medicine, National Health Research Institutes, Miaoli County, Taiwan, Republic of China.

Abstract

BACKGROUND: 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.

METHODOLOGY AND PRINCIPAL FINDINGS: We applied Cre/loxP system to generate conditional gene targeted mice that allow inactivation of critical components of Notch signaling pathway in the skin. Rbpj, the core component of all four Notch receptors, and Pofut1, an essential factor for ligand-receptor interactions, were inactivated in hair follicle lineages and suprabasal layer of the epidermis using the Tgfb3-Cre mouse line. Rbpj conditional inactivation resulted in granular parakeratosis and reactive epidermal hyperplasia. Pofut1 conditional inactivation led to ultrastructural abnormalities in the granular layer and altered filaggrin processing in the epidermis, suggesting a perturbation of the granular layer differentiation. Disruption of Pofut1 in hair follicle lineages resulted in aberrant telogen morphology, a decrease of bulge stem cell markers, and a concomitant increase of K14-positive keratinocytes in the isthmus of mutant hair follicles. Pofut1-deficent hair follicles displayed a delay in anagen re-entry and dysregulation of proliferation and apoptosis during the hair cycle transition. Moreover, increased DNA double stand breaks were detected in Pofut1-deficent hair follicles, and real time PCR analyses on bulge keratinocytes isolated by FACS revealed an induction of DNA damage response and a paucity of DNA repair machinery in mutant bulge keratinocytes.

SIGNIFICANCE: 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.

PMID: 21267458 http://www.ncbi.nlm.nih.gov/pubmed/21267458

2009

The role of Notch in patterning the human vertebral column

Curr Opin Genet Dev. 2009 Aug;19(4):329-37. Epub 2009 Jul 14.

Dunwoodie SL. Source Developmental Biology Division, Victor Chang Cardiac Research Institute, 405 Liverpool Street, Darlinghurst, NSW 2010 Sydney, Australia. s.dunwoodie@victorchang.edu.au <s.dunwoodie@victorchang.edu.au> Abstract The components of the Notch signaling pathway and the mechanics of signal transduction have largely been established in Drosophila. Although essential for many developmental processes in invertebrates and vertebrates, this review focuses on Notch signaling in the vertebrate-specific process of somitogenesis. More specifically it describes that mutations in genes encoding Notch pathway components (DLL3, MESP2, LFNG and HES7) cause severe congenital vertebral defects in humans. Importantly, this review highlights studies demonstrating that Dll3 is unique amongst DSL ligands acting as an inhibitor and not an activator of Notch signaling.

PMID: 19608404 http://www.ncbi.nlm.nih.gov/pubmed/19608404