A genetic analysis of the cytological region 46C-F containing the Drosophila melanogaster homolog of the jun proto-oncogene

Abstract

The cytogenetic region 46C-F on the right arm of Drosophila chromosome 2, which contains the homolog of the human jun proto-oncogene, has been genetically mapped and characterized. This project led to the identification and characterization of a Jra (jun-related antigen) mutation, which has been described in detail elsewhere. Three mutagens, EMS, DEB and gamma-rays, were used to isolate 126 lethal lines for this interval. Complementation analysis of the 126 lethal lines identified 29 lethal complementation groups in the region; nine of which have now been correlated with known genes or phenotypes. The region has been subdivided into ten intervals using various small deletions, seven intervals in 46C/D and three intervals in 46E/F. Sixteen P-element lines have been mapped to this interval and are allelic to eight of our complementation groups. The remaining unidentified complementation groups have been analyzed for critical phase, which is when the first observable defect arises and/or when death occurs. There are twelve embryonic lethal groups and seven larval lethal groups. Three lines show visible abnormalities in gut and tracheal development prior to death.

A mosaic genetic screen for genes necessary forDrosophilamushroom body neuronal morphogenesis

“…Deficiency mapping for 7A11 uncovered two lethal mutations at 46E1-F2 and 54C1-4. Of the 29 lethal complementation groups from a previous saturation mutagenesis in the 46C-F region (Goldstein et al, 2001), two alleles in group W failed to complement 7A11. However, when recombined with FRTG13, they did not exhibit a clonal phenotype in MB neurons.…”

Neuronal remodeling and apoptosis require VCP-dependent degradation of the apoptosis inhibitor DIAP1

“…UAS-tau::GFP was a gift of W. Song (University of California, San Francisco, CA, USA); other lines included UAS-mCD8GFP (Lee and Luo, 1999), UAS-dVCP-IR (inverted repeat, VDRC 24354) and UAS-dcr2 (Dietzl et al, 2007), UAS-p35 (Hay et al, 1994) (Bloomington) and UAS-mCD8::PARP::Venus (Williams et al, 2006). Mutant alleles included dvcp and dvcp [7][8][9][10][11][12] (Goldstein et al, 2001;Ruden et al, 2000) and th 4 (Hay et al, 1995) (all from Bloomington).…”

“…1E-H). In order to increase the strength and penetrance of potential VCP loss-of-function phenotypes in class IV neurons, we either expressed VCP RNAi in a heterozygous dvcp [7][8][9][10][11][12] /+ mutant background (Goldstein et al, 2001) or used two copies of the UAS-VCP QQ transgene. Whereas the heterozygous mutations did not visibly affect the ddaC neuron (Fig.…”

A Molecular Mechanism of Temperature Sensitivity for Mutations Affecting the Drosophila Muscle Regulator Myocyte Enhancer Factor-2

“…We therefore tested the viability of mutants heteroallelic for 30-5 and the Mef2 null allele P544 (Lilly et al 1995). Since P544 was isolated in a different genetic screen to the Goldstein et al (2001) alleles, the P544 chromosome is unlikely to share any second-site lethal mutations with 30-5. We found in this instance that 13% of 30-5/P544 mutants survived to adulthood at the permissive temperature (12 observed out of 89 expected) but none survived at the restrictive temperature (0 observed, 238 expected).…”

“…Mef2 mutants were obtained from Elliot Goldstein (Arizona State University; Goldstein et al 2001) and balanced over a CyO, Cy Kr-GFP balancer chromosome (Casso et al 1999). Viability studies were achieved by crossing CyO, Cy Kr-GFP/Mef2…”