Ectopic expression of the Drosophila tramtrack gene results in multiple embryonic defects, including repression of even-skipped and fushi tarazu

Douglas Read, Michael Levine, James L. Manley

Research output: Contribution to journalArticle

44 Scopus citations

Abstract

The tramtrack (ttk) gene of Drosophila encodes 69-kDa and 88-kDA proteins through alternative splicing of the primary ttk transcript. The two proteins share a common amino-terminal sequence, but contain different carboxy-terminal portions, each of which has a distinct zinc finger domain with a unique DNA binding specificity. The 69-kDa ttk protein has been shown to bind multiple sites within important regulatory elements of the pair-rule genes even-skipped (eve) and fushi tarazu (ftz), and it has been suggested that this protein may function as a repressor of ftz transcription. Here we present evidence that the 69-kDa ttk protein can indeed repress expression not only of ftz, but also of eve. Ectopic expression of the 69-kDa protein, but not of the 88-kDa form, was found to nearly abolish the striped patterns of expression of both eve and ftz in transgenic embryos. These findings, coupled with our detection of significant levels of ttk protein in ovaries and 0-2-h embryos, support the idea that maternally supplied ttk protein to prevent premature activation of eve and ftz, thereby helping to establish the timing of the onset of zygotic expression of these two genes. Furthermore, gross defeects in larval cuticle resulting from misexpression of the 69-kDa protein suggest that this protein performs additional functions in the early embryos.

Original languageEnglish (US)
Pages (from-to)183-195
Number of pages13
JournalMechanisms of Development
Volume38
Issue number3
DOIs
StatePublished - Sep 1992
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Embryology
  • Developmental Biology

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