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EMBO J. 1991 Feb;10(2):407-17.

Retrotransposon-induced overexpression of a homeobox gene causes defects in eye morphogenesis in Drosophila.

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Department of Biology, Johns Hopkins University, Baltimore, MD 21218.


Insertion of the tom transposable element into various Drosophila ananassae genes results in dominant phenotypes that affect eye morphology. One of these genes encoded by the Om(1D) locus was isolated by transposon tagging. The Om(1D) gene encodes a 2.7 kb transcript that is expressed in every stage of development. The deduced Om(1D) protein is 606 amino acids long and contains two glutamine/histidine, two alanine-rich and one histidine/proline repeats, as well as a homeodomain located near the carboxy terminus. Tom-induced alleles of Om(1D) show a 1.7-fold increased accumulation of Om(1D) RNA in whole individuals during late larval--early pupal stages of development, whereas expression of this transcript is 7-fold higher in the eye--antenna imaginal disc of mutant versus wild-type flies. D. melanogaster flies transformed with the Om(1D) coding region under the control of the hsp70 promoter display an eye phenotype similar to that of Om(1D) when expression of the homeobox protein encoded by the chimeric gene is induced by temperature elevation at the end of the third instar period. These results suggest that the eye-specific mutant phenotype caused by the insertion of the tom retrotransposon in the Om(1D) locus may be a consequence of the tissue-specific induction of the expression of this gene by sequences present in the transposable element.

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