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Titolo:
The transcription factor FoxH1 (FAST) mediates Nodal signaling during anterior-posterior patterning and node formation in the mouse
Autore:
Yamamoto, M; Meno, C; Sakai, Y; Shiratori, H; Mochida, K; Ikawa, Y; Saijoh, Y; Hamada, H;
Indirizzi:
Osaka Univ, Inst Mol & Cellular Biol, Div Mol Biol, Osaka 5650871, Japan Osaka Univ Osaka Japan 5650871 Biol, Div Mol Biol, Osaka 5650871, Japan Japan Sci & Technol Corp, CREST, Osaka 5650871, Japan Japan Sci & Technol Corp Osaka Japan 5650871 CREST, Osaka 5650871, Japan
Titolo Testata:
GENES & DEVELOPMENT
fascicolo: 10, volume: 15, anno: 2001,
pagine: 1242 - 1256
SICI:
0890-9369(20010515)15:10<1242:TTFF(M>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
RIGHT ASYMMETRIC EXPRESSION; TGF-BETA SUPERFAMILY; VISCERAL ENDODERM; PRIMITIVE ENDODERM; EMBRYO; GASTRULATION; HEAD; ORGANIZER; ZEBRAFISH; PROTEIN;
Keywords:
anterior-posterior patterning; FoxH1; gastrulation; Nodal; node;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
64
Recensione:
Indirizzi per estratti:
Indirizzo: Hamada, H Osaka Univ, Inst Mol & Cellular Biol, Div Mol Biol, Osaka 5650871, Japan Osaka Univ Osaka Japan 5650871 Mol Biol, Osaka 5650871, Japan
Citazione:
M. Yamamoto et al., "The transcription factor FoxH1 (FAST) mediates Nodal signaling during anterior-posterior patterning and node formation in the mouse", GENE DEV, 15(10), 2001, pp. 1242-1256

Abstract

FoxH1 (FAST) is a transcription factor that mediates signaling by transforming growth factor-beta, Activin, and Nodal. The role of FoxH1 in development has now been investigated by the generation and analysis of FoxH1-deficient (FoxH1(-/-)) mice. The FoxH1(-/-) embryos showed various patterning defects that recapitulate most of the defects induced by the loss of Nodal signaling. A substantial proportion of FoxH1(-/-) embryos failed to orient theanterior-posterior (A-P) axis correctly, as do mice lacking Cripto, a coreceptor for Nodal. In less severely affected FoxH1(-/-) embryos, A-P polarity was established, but the primitive streak failed to elongate, resulting in the lack of a definitive node and its derivatives. Heterozygosity for nodal renders the FoxH1(-/-) phenotype more severe, indicative of a genetic interaction between FoxH1 and nodal. The expression of FoxH1 in the primitiveendoderm rescued the A-P patterning defects, but not the midline defects, of FoxH1(-/-) mice. These results indicate that a Nodal-FoxH1 signaling pathway plays a central role in A-P patterning and node formation in the mouse.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/03/20 alle ore 10:11:52