Epiblast-specific loss of HCF-1 leads to failure in anterior-posterior axis specification.

Détails

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Etat: Public
Version: de l'auteur
ID Serval
serval:BIB_D6717D629178
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Epiblast-specific loss of HCF-1 leads to failure in anterior-posterior axis specification.
Périodique
Developmental Biology
Auteur(s)
Minocha S., Bessonnard S., Sung T.L., Moret C., Constam D.B., Herr W.
ISSN
1095-564X (Electronic)
ISSN-L
0012-1606
Statut éditorial
Publié
Date de publication
2016
Peer-reviewed
Oui
Volume
91
Numéro
4
Pages
294-297
Langue
anglais
Résumé
Mammalian Host-Cell Factor 1 (HCF-1), a transcriptional co-regulator, plays important roles during the cell-division cycle in cell culture, embryogenesis as well as adult tissue. In mice, HCF-1 is encoded by the X-chromosome-linked Hcfc1 gene. Induced Hcfc1(cKO/+) heterozygosity with a conditional knockout (cKO) allele in the epiblast of female embryos leads to a mixture of HCF-1-positive and -deficient cells owing to random X-chromosome inactivation. These embryos survive owing to the replacement of all HCF-1-deficient cells by HCF-1-positive cells during E5.5 to E8.5 of development. In contrast, complete epiblast-specific loss of HCF-1 in male embryos, Hcfc1(epiKO/Y), leads to embryonic lethality. Here, we characterize this lethality. We show that male epiblast-specific loss of Hcfc1 leads to a developmental arrest at E6.5 with a rapid progressive cell-cycle exit and an associated failure of anterior visceral endoderm migration and primitive streak formation. Subsequently, gastrulation does not take place. We note that the pattern of Hcfc1(epiKO/Y) lethality displays many similarities to loss of β-catenin function. These results reveal essential new roles for HCF-1 in early embryonic cell proliferation and development.
Mots-clé
Aged, Carcinoid Tumor/diagnosis, Diagnosis, Differential, Humans, Jejunal Neoplasms/diagnosis, Laparotomy, Male, Whipple Disease/diagnosis
Pubmed
Web of science
Open Access
Oui
Création de la notice
15/09/2016 21:25
Dernière modification de la notice
20/08/2019 16:56
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