Research

A rapid method to map mutations in Drosophila

Sophie G Martin¹, Krista C Dobi^1,2 and Daniel St Johnston¹

¹  Wellcome/CRC Institute, Tennis Court Road, Cambridge CB2 1QR, UK

²  Harvard Medical School, 25 Shattuck Street, Boston, MA 02115, USA

author email corresponding author email

Genome Biology 2001, 2:research0036.1-0036.12doi:10.1186/gb-2001-2-9-research0036

Published:	30 August 2001

Subject areas: Genetics, Genome studies, Methods, Model organisms

Abstract

Background

Genetic screens in Drosophila have provided a wealth of information about a variety of cellular and developmental processes. It is now possible to screen for mutant phenotypes in virtually any cell at any stage of development by performing clonal screens using the flp/FRT system. The rate-limiting step in the analysis of these mutants is often the identification of the mutated gene, however, because traditional mapping strategies rely mainly on genetic and cytological markers that are not easily linked to the molecular map.

Results

Here we describe the development of a single-nucleotide polymorphism (SNP) map for chromosome arm 3R. The map contains 73 polymorphisms between the standard FRT chromosome, and a mapping chromosome that carries several visible markers (rucuca), at an average density of one SNP per 370 kilobases (kb). Using this collection, we show that mutants can be mapped to a 400 kb interval in a single meiotic mapping cross, with only a few hundred SNP detection reactions. Discovery of further SNPs in the region of interest allows the mutation to be mapped with the same recombinants to a region of about 50 kb.

Conclusion

The combined use of standard visible markers and molecular polymorphisms in a single mapping strategy greatly reduces both the time and cost of mapping mutations, because it requires at least four times fewer SNP detection reactions than a standard approach. The use of this map, or others developed along the same lines, will greatly facilitate the identification of the molecular lesions in mutants from clonal screens.