Molecular lesions associated with white gene mutations induced by I-R hybrid dysgenesis in Drosophila melanogaster

• Published in: The EMBO journal Vol. 3; no. 13; pp. 3079 - 3085
• Main Authors: Sang, H.M, Pelisson, A, Bucheton, A, Finnegan, D.J
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group 20.12.1984
• Subjects: Applied sciences; Drosophila melanogaster; Drosophilidae; Exact sciences and technology; genes; hybrid dysgenesis; mutation; Other techniques and industries; transposable elements; white gene
• ISSN: 0261-4189; 1460-2075
• DOI: 10.1002/j.1460-2075.1984.tb02262.x

We have identified molecular lesions associated with six mutations, wIR2 and wIR4‐8, of the white gene of Drosophila melanogaster. These mutations arose in flies subject to I‐R hybrid dysgenesis. Four of the mutations give rise to coloured eyes and are associated with insertions of 5.4‐kb elements indistinguishable from the I factor controlling I‐R dysgenesis. The insertion associated with wIR4 is at a site which, within the resolution of these experiments, is identical to that of two previously studied I factors. This appears to be a hot‐spot for I factor insertion. We have compared the sites of these insertions with sequences complementary to white gene mRNA identified by Pirrotta and Bröckl. The hot‐spot is in the fourth intron. The insertion carried by wIR5 is either within, or just beyond, the last exon. The insertion carried by wIR6 is near the junction of the first exon and first intron. The wIR2 mutation is a derivative of w1. It contains an insertion of I factor DNA within, or immediately adjacent to, the F‐like element associated with w1, and results in restoration of some eye colour. This insertion is just upstream of the start of the white mRNA. Mutations wIR7 and wIR8 are deletions removing mRNA coding sequences. Both determine a bleached white phenotype.