The pioneer gene, apontic, is required for morphogenesis and function of the Drosophila heart

Ming Tsan Su, Tyamagondlu V. Venkatesh, Xuishan Wu, Krista Golden, Rolf Bodmer*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

19 Citations (Scopus)


In an effort to isolate genes required for heart development and to further our understanding of cardiac specification at the molecular level, we screened PlacZ enhancer trap lines for expression in the Drosophila heart. One of the lines generated in this screen, designated B2-2-15, was particularly interesting because of its early pattern of expression in cardiac precursor cells, which is dependent on the homeobox gene tinman, a key determinant of heart development in Drosophila. We isolated and characterized a gene in the vicinity of B2-2-15 that exhibits an identical expression pattern than the reporter gene of the enhancer trap. The product of his gene, apontic (apt; see also Gellon et al., 1997), does not appear to have any homology with known genes. apt mutant embryos show distinct abnormalities in heart morphology as early as mid-embryonic stages when the heat tube assembles, in that segments of heart cells (those of myocardial and pericardial identity) are often missing. Most strikingly, however, apt mutant embryos or larvae only develop a much reduced heart rate, perhaps because of defects in the assembly of an intact heart tube and/or because of defects in the function or physiological control of the myocardial cells, which normally mediate heart contractions. These cardiac defects may be the cause of death of these mutants during late embryonic or early larval stages.

Original languageEnglish
Pages (from-to)125-132
Number of pages8
JournalMechanisms of Development
Issue number2
Publication statusPublished - 1999 Feb
Externally publishedYes


  • Apontic
  • Cardiogenesis
  • Drosophila
  • Enhancer trap
  • Heart morphogenesis
  • Heartbeat
  • Mesoderm

ASJC Scopus subject areas

  • Embryology
  • Developmental Biology


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