192 Oral - Techniques and Technology Session
Saturday April 09, 4:00 PM - 4:15 PM

Enabling recombination on the 4th chromosome: FRT101F and Bloom syndrome helicase


Authors:
Stuart Newfeld 1; Mary Jane O'Connor 2; Samuel Goldsmith 1; Petra Tauscher 3; Samantha Daly 1; Osamu Shimmi 3,4; Michael O'Connor 2

Affiliations:
1) School of Life Sciences, Arizona State University, Tempe AZ ; 2) Dept. Genetics, Cell Biology and Development, Univ. Minnesota, Minneapolis, MN; 3) Institute of Biotechnology, University of Helsinki, Helsinki, Finland; 4) Institute of Molecular and Cell Biology, University of Tartu, Tartu, Estonia

Keywords:
f. recombination systems; l. Insulin signaling/ insulin-like peptides

Genes on the long arm of the Drosophila 4th chromosome are difficult to study because the chromosome lacks mitotic and meiotic recombination. Without recombination it is not possible to employ clonal analysis - the creation of a single mutant cell at a specific time and place followed by the phenotypic examination of its descendants. Here we report new resources for the 4th chromosome. For mitotic recombination we generated a chromosome with an FRT very near the centromere in 101F and a derivative that carries FRT101F with a distal ubiquitously expressed GAL80 transgene. This pair of chromosomes enables both unmarked and MARCM clones. An example from the IPC neurons of the brain is shown. For meiotic recombination we demonstrate that a Bloom syndrome helicase and recombination defective double mutant genotype can create recombinant 4th chromosomes via female meiosis. An example creating a w+ and y+ chromosome is shown. An efficient method for X to 4th transposition is also described. These chromosomes and strategies should accelerate the genetic analysis of protein coding genes on the 4th chromosome, including the 44 genes with no demonstrated function. Studies of these well conserved genes will close gaps in our knowledge of development and physiology.