Towards Understanding the Gene-Specific Roles of GATA Factors in Heart Development: Does GATA4 Lead the Way?

Boni A. Afouda* (Corresponding Author)

*Corresponding author for this work

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Abstract

Transcription factors play crucial roles in the regulation of heart induction, formation, growth and morphogenesis. Zinc finger GATA transcription factors are among the critical regulators of these processes. GATA4, 5 and 6 genes are expressed in a partially overlapping manner in developing hearts, and GATA4 and 6 continue their expression in adult cardiac myocytes. Using different experimental models, GATA4, 5 and 6 were shown to work together not only to ensure specification of cardiac cells but also during subsequent heart development. The complex involvement of these related gene family members in those processes is demonstrated through the redundancy among them and crossregulation of each other. Our recent identification at the genome-wide level of genes specifically regulated by each of the three family members and our earlier discovery that gata4 and gata6 function upstream, while gata5 functions downstream of noncanonical Wnt signalling during cardiac differentiation, clearly demonstrate the functional differences among the cardiogenic GATA factors. Such suspected functional differences are worth exploring more widely. It appears that in the past few years, significant advances have indeed been made in providing a deeper understanding of the mechanisms by which each of these molecules function during heart development. In this review, I will therefore discuss current evidence of the role of individual cardiogenic GATA factors in the process of heart development and emphasize the emerging central role of GATA4.
Original languageEnglish
Article number5255
Number of pages20
Journal International Journal of Molecular Sciences
Volume23
Issue number9
Early online date9 May 2022
DOIs
Publication statusPublished - 9 May 2022

Keywords

  • transcription factors
  • heart development
  • GATA4 genes
  • noncanonical Wnt Signalling

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