717B Poster - 11. Cell division and cell growth
Friday April 08, 2:00 PM - 4:00 PM

Molecular genetic analysis of the mutation I.3.2 by undergraduates participating in a Drosophila CURE


Authors:
Cory Evans 1; Veronica Casarez 1; Kayla Bieser 2; Jacob Kagey 3

Affiliations:
1) Loyola Marymount University; 2) Nevada State College; 3) University of Detroit Mercy

Keywords:
q. developmental modulation; f. classroom undergraduate research experience (CURE)

The mutation I.3.2 was identified in an FLP/FRT-based genetic screen for novel regulators of cell growth located on the right arm of chromosome 2 (2R). Because abnormal growth phenotypes associated with new mutations may be suppressed by the parallel activation of apoptosis, EMS was used to mutagenize an FRT42D chromosome already carrying the Dark82 mutation, which strongly suppresses apoptosis. This screen successfully identified several new mutations affecting cell growth including I.3.2. Some of these mutations have been or are being characterized by undergraduate students participating in FlyCURE, a course-based undergraduate research experience (CURE) that is being implemented at several partnering colleges and universities across the country. Here we describe the FlyCURE analysis of mutation I.3.2., which behaves zygotically as a recessive lethal. I.3.2 is likely also a cell-lethal mutation, as flies with mitotic mutant clones created in the developing eye (using ey-FLP) are pupal lethal and exhibit an almost complete lack of developing head structures. Complementation mapping of the I.3.2 recessive-lethal phenotype using the Bloomington Drosophila Stock Center 2R Deficiency Kit identified two non-complementing deficiencies. These deficiencies overlap in the cytological interval 50A7-50A13, a small chromosomal region containing thirteen genes. A lethal allele of one of these genes, centromere identifier (cid), failed to complement I.3.2, suggesting that I.3.2 is an allele of cid. DNA sequence analysis of the cid locus in the I.3.2 genetic background is underway to confirm the identity of the I.3.2 gene and determine the molecular nature of the mutation.