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PMID:19035347

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Citation

Vincentz, JW, Barnes, RM, Firulli, BA, Conway, SJ and Firulli, AB (2008) Cooperative interaction of Nkx2.5 and Mef2c transcription factors during heart development. Dev. Dyn. 237:3809-19

Abstract

The interactions of diverse transcription factors mediate the molecular programs that regulate mammalian heart development. Among these, Nkx2.5 and the Mef2c regulate common downstream targets and exhibit striking phenotypic similarities when disrupted, suggesting a potential interaction during heart development. Co-immunoprecipitation and mammalian two-hybrid experiments revealed a direct molecular interaction between Nkx2.5 and Mef2c. Assessment of mRNA expression verified spatiotemporal cardiac coexpression. Finally, genetic interaction studies employing histological and molecular analyses showed that, although Nkx2.5(-/-) and Mef2c(-/-) individual mutants both have identifiable ventricles, Nkx2.5(-/-);Mef2c(-/-) double mutants do not, and that mutant cardiomyocytes express only atrial and second heart field markers. Molecular marker and cell death and proliferation analyses provide evidence that ventricular hypoplasia is the result of defective ventricular cell differentiation. Collectively, these data support a hypothesis where physical, functional, and genetic interactions between Nkx2.5 and Mef2c are necessary for ventricle formation.

Links

PubMed PMC2639719 Online version:10.1002/dvdy.21803

Keywords

Animals; Cell Differentiation; Cell Line; Gene Expression Regulation, Developmental; Heart/embryology; Homeodomain Proteins/genetics; Homeodomain Proteins/immunology; Humans; Mice; Mice, Knockout; Mutation/genetics; Myocardium/cytology; Myocardium/metabolism; Myogenic Regulatory Factors/genetics; Myogenic Regulatory Factors/immunology; Protein Binding; Transcription Factors/deficiency; Transcription Factors/genetics; Transcription Factors/immunology

Significance

Annotations

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

MOUSE:NKX25

acts_upstream_of_or_within

GO:0003211: cardiac ventricle formation

ECO:0000316: genetic interaction evidence used in manual assertion

MGI:MGI:99458

P

  • results_in_formation_of:(EMAPA:16350)

Seeded From UniProt

complete

MOUSE:NKX25

acts_upstream_of_or_within

GO:0003151: outflow tract morphogenesis

ECO:0000316: genetic interaction evidence used in manual assertion

MGI:MGI:99458

P

Seeded From UniProt

complete

MOUSE:NKX25

acts_upstream_of_or_within

GO:0055007: cardiac muscle cell differentiation

ECO:0000316: genetic interaction evidence used in manual assertion

MGI:MGI:99458

P

  • occurs_in:(EMAPA:16353)

Seeded From UniProt

complete

MOUSE:MEF2C

acts_upstream_of_or_within

GO:0003211: cardiac ventricle formation

ECO:0000316: genetic interaction evidence used in manual assertion

MGI:MGI:97350

P

  • results_in_formation_of:(EMAPA:16350)

Seeded From UniProt

complete

MOUSE:MEF2C

acts_upstream_of_or_within

GO:0003151: outflow tract morphogenesis

ECO:0000316: genetic interaction evidence used in manual assertion

MGI:MGI:97350

P

Seeded From UniProt

complete

MOUSE:MEF2C

acts_upstream_of_or_within

GO:0090073: positive regulation of protein homodimerization activity

ECO:0000314: direct assay evidence used in manual assertion

P

Seeded From UniProt

complete

MOUSE:MEF2C

acts_upstream_of_or_within

GO:0055007: cardiac muscle cell differentiation

ECO:0000316: genetic interaction evidence used in manual assertion

MGI:MGI:97350

P

  • occurs_in:(EMAPA:16353)
  • results_in_acquisition_of_features_of:(CL:0000746)

Seeded From UniProt

complete

MOUSE:MEF2C

acts_upstream_of_or_within

GO:0003211: cardiac ventricle formation

ECO:0000316: genetic interaction evidence used in manual assertion

MGI:MGI:97350

P

results_in_formation_of:(EMAPA:16350)

Seeded From UniProt

complete

MOUSE:MEF2C

acts_upstream_of_or_within

GO:0003151: outflow tract morphogenesis

ECO:0000316: genetic interaction evidence used in manual assertion

MGI:MGI:97350

P

has_participant:(EMAPA:16346)

Seeded From UniProt

complete


See also

References

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