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Induction of epithelial tumors in Drosophila melanogaster heterozygous for the tumor suppressor gene wts
Author(s) -
Eeken Jan C.J.,
Klink Ilse,
van Veen Bert L.,
Pastink Albert,
Ferro Wouter
Publication year - 2002
Publication title -
environmental and molecular mutagenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 87
eISSN - 1098-2280
pISSN - 0893-6692
DOI - 10.1002/em.10119
Subject(s) - drosophila melanogaster , biology , mutagen , imaginal disc , mutation , somatic cell , drosophilidae , genetics , phenotype , compound eye , gene , tumor suppressor gene , methyl methanesulfonate , microbiology and biotechnology , cell , carcinogenesis , carcinogen , dna repair , physics , optics
The imaginal disk cells of Drosophila have a cell cycle that is very similar to that of mammalian cells. Data concerning factors inducing tumors in these cells may directly relate to the risk of these factors for inducing cancer in humans. One of the genes involved in the regulation of cell cycle control is wts ( warts ), the Drosophila homolog of the mammalian tumor suppressor gene LATS1. The Drosophila wts mutations are recessive lethal. However, homozygous clones that arise in heterozygous flies in the imaginal disk cells lead to epithelial tumors, spectacular outgrowths visible on the cuticle of the adult. We have treated Drosophila larvae, heterozygous for wts , with the chemical mutagen MMS (methyl methanesulfonate) or with X‐rays and measured the appearance of epithelial tumors in the eclosing adult flies. This test is a variation of the well‐known Drosophila somatic mutation and recombination test (SMART), where mostly recessive markers have been used leading to visible phenotypes in the eyes and wings of the fly. We show that the sensitivity of this test is far greater than the comparable test system using the recessive eye marker white . Environ. Mol. Mutagen. 40:277–282, 2002. © 2002 Wiley‐Liss, Inc.