PuSH - Publikationsserver des Helmholtz Zentrums München: Gsk3 beta/PKA and Gli1 regulate the maintenance of neural progenitors at the midbrain-hindbrain boundary in concert with E(Spl) factor activity.

Informationen

Hinweise zu Qualitätskriterien von Zeitschriften

Open-Access-Richtlinie der Helmholtz-Gemeinschaft 2016

CC Licencences

Metriken für Publikationen

Navigation

Startseite

English

EVA: Veröffentlichen

Neuer EVA Antrag

Recherche

Erweiterte Suche

Durchblättern nach ...

... HMGU-Autoren/Konsortien

... Organisationsstruktur

... Zeitschriften

... Publikationstypen

... Forschungsdaten

... Arbeitsgruppen

... Erscheinungsjahr

Publikationen im Überblick

Statistik

HGF Fortschrittsbericht

OA Publikationen

Eintragen

Neue Publikation eintragen

Neue Publikation holen aus...

...EVA

Fehlende Publikation melden

Highlights

Suche

Hilfe & Kontakt

Ansprechpartner

Hilfe

Datenschutz

Helmholtz Open Science

Bibliometrische Indikatoren

SHERPA/RoMEO

DOAJ

Export:

Text

Endnote (RIS) BIB

BibTeX

Ninkovic, J. ; Stigloher, C. ; Lillesaar, C. ; Bally-Cuif, L.

Gsk3 beta/PKA and Gli1 regulate the maintenance of neural progenitors at the midbrain-hindbrain boundary in concert with E(Spl) factor activity.

Development 135, 3137-3148 (2008)

DOI

Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.

Abstract
Metriken
Zusatzinfos

Neuronal production in the midbrain-hindbrain domain (MH) of the vertebrate embryonic neural tube depends on a progenitor pool called the 'intervening zone' (IZ), located at the midbrain-hindbrain boundary. The progressive recruitment of IZ progenitors along the mediolateral (future dorsoventral) axis prefigures the earlier maturation of the MH basal plate. It also correlates with a lower sensitivity of medial versus lateral IZ progenitors to the neurogenesis inhibition process that maintains the IZ pool. This role is performed in zebrafish by the E(Spl) factors Her5 and Her11, but the molecular cascades cooperating with Her5/11, and those accounting for their reduced effect in the medial IZ, remain unknown. We demonstrate here that the kinases Gsk3 beta and cAMP-dependent protein kinase A (PKA) are novel determinants of IZ formation and cooperate with E( Spl) activity in a dose-dependent manner. Similar to E(Spl), we show that the activity of Gsk3 beta/PKA is sensed differently by medial versus lateral IZ progenitors. Furthermore, we identify the transcription factor Gli1, expressed in medial IZ cells, as an antagonist of E(Spl) and Gsk3 beta/ PKA, and demonstrate that the neurogenesis-promoting activity of Gli1 accounts for the reduced sensitivity of medial IZ progenitors to neurogenesis inhibitors and their increased propensity to differentiate. We also show that the expression and activity of Gli1 in this process are, surprisingly, independent of Hedgehog signaling. Together, our results suggest a model in which the modulation of E(Spl) and Gsk3 beta/PKA activities by Gli1 underlies the dynamic properties of IZ maintenance and recruitment.

Impact Factor

Scopus SNIP

Web of Science
Times Cited

Scopus
Cited By

Altmetric

7.293

2.340