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PMID:18955134

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Citation

Raid, R, Krinka, D, Bakhoff, L, Abdelwahid, E, Jokinen, E, Kärner, M, Malva, M, Meier, R, Pelliniemi, LJ, Ploom, M, Sizarov, A, Pooga, M and Karis, A Lack of Gata3 results in conotruncal heart anomalies in mouse. Mech. Dev. 126:80-9

Abstract

The transcription factor Gata3 is an important regulator of the development of thymus, the nervous system, ear, kidney, and adrenal glands. This study analyzes the role of Gata3 in the developing heart using a mouse strain containing an nlsLacZ reporter gene fused in frame to the Gata3 gene by homologous recombination. Using in situ hybridization, RT-PCR and Gata3-LacZ histochemistry, Gata3 expression was shown in various cardiac structures up to newborn stage. During looping stages (E9.5-E11.5) Gata3-LacZ activity recapitulated endogenous Gata3 and was abundantly expressed in the endocardial ridges and endothelium of distal outflow tract. Strong reporter gene expression was also noted in the mesenchyme of ventral branchial arches, and in the epithelium. In the atrioventricular canal expression was relatively lower. In the four-chambered heart stages (E13.5-E17.5) the LacZ-staining did not recapitulate the endogenous Gata3 transcript and showed rather lineage tracing of formerly Gata3-expressing cells in the hearts. beta-Galactosidase activity was detected in the cusps of semilunar valves, aorta, pulmonary trunk, innominate and common carotid arteries, and faintly in the atrioventricular valves. Gata3-null embryos die normally between E11 and E12. Pharmacological treatment with sympathomimetic beta-adrenergic receptor agonist lengthens the survival up to E18 when malformations of the heart such as ventricular septal defect (VSD), double-outlet of right ventricle (DORV), anomalies of the aortic arch (AAA) and persistent truncus arteriosus (PTA) were detected. The specified malformations correlate with the normal developmental pattern of Gata3-LacZ expression. The short outflow tract and insufficient rotation of truncus arteriosus during looping stages might be the main reasons underlying these malformations.

Links

PubMed Online version:10.1016/j.mod.2008.10.001

Keywords

Animals; Embryo, Mammalian/embryology; Embryo, Mammalian/metabolism; GATA3 Transcription Factor/deficiency; GATA3 Transcription Factor/genetics; GATA3 Transcription Factor/metabolism; Gene Expression Regulation, Developmental; Genes, Reporter/genetics; Heart Defects, Congenital/genetics; Heart Defects, Congenital/metabolism; Heart Defects, Congenital/physiopathology; In Situ Hybridization; Mice; Mice, Knockout; Neural Crest/embryology; Neural Crest/metabolism; Phenotype; RNA, Messenger/genetics

Significance

Annotations

Gene product Qualifier GO Term Evidence Code with/from Aspect Extension Notes Status

MOUSE:GATA3

involved_in

GO:0003180: aortic valve morphogenesis

ECO:0000315: mutant phenotype evidence used in manual assertion

P

Seeded From UniProt

complete

MOUSE:GATA3

involved_in

GO:0003215: cardiac right ventricle morphogenesis

ECO:0000315: mutant phenotype evidence used in manual assertion

P

Seeded From UniProt

complete

MOUSE:GATA3

involved_in

GO:0003281: ventricular septum development

ECO:0000315: mutant phenotype evidence used in manual assertion

P

Seeded From UniProt

complete

MOUSE:GATA3

involved_in

GO:0060037: pharyngeal system development

ECO:0000315: mutant phenotype evidence used in manual assertion

P

Seeded From UniProt

complete


See also

References

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