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In Drosophila melanogaster genetic screens are often used to identify genes associated with different biological processes. Here, we have utilized the Flp/FRT system to generate mitotic clones within the developing eye. These clones were screened for mutations that disrupt cell division, organ patterning, and cell growth. One such mutation from this screen, mutant M.3.2, resulted in an expansion of the cuticle within the area normally covered by ommatidium as well as an overall smaller eye size. Genetic and molecular mapping revealed this mutation to be in the gene, tout-velu (ttv). 

The multi-institutional Fly-CURE project is an undergraduate genetics research initiative centered on Drosophila melanogaster as a model organism. This study aimed to characterize and map mutations discovered through a Flp/FRT EMS screen to investigate complex interactions among genes associated with cell division, growth, and apoptosis leading to abnormal cell proliferation. The F.1.1 mosaic phenotype resulted in a rough eye phenotype with an overall decrease in representation of mutant tissue. To genetically map the location of the F.1.1 mutation, flies with genotype FRT42D,F.1.1,Dark⁸²/CyO were crossed with the Bloomington 2R Deficiency Kit. The resultant F1 progeny were analyzed to pinpoint mapping deficiencies. The genomic region containing the Patronin gene was identified and sequencing confirmed the novel allele of Patronin^F.1.1. 

The E.3.3 mutation was generated in a Flp/FRT EMS screen for conditional mutations that cause growth and developmental defects in a genetic background that blocks apoptosis. The mutations were conditional, based on the Dark⁸²allele being present on the starting chromosome, and blocking canonical apoptosis in a homozygous state. The E.3.3 mosaic eyes exhibit defects in eye development including patches of rough eye and irregular surface structure. Whole Genome Sequencing and complementation mapping revealed E.3.3 as an allele of prod. Prod is a DNA-binding protein that binds satellite repeats and is involved in chromocenter formation during mitosis. Here we present a novel allele of prod, prod^E.3.3, that disrupts the functional region of the Prod protein resulting in disruption of typical eye structure, likely due to disruption of chromatid separation during development. 

Genetic screens are valuable for identifying novel genes involved in the regulation of developmental processes. To identify genes associated with cell growth regulation in Drosophila melanogaster, a mutagenesis screen was performed. Undergraduate students participating in Fly-CURE phenotypically characterized the E.4.1 mutant which is associated with rough eyes and antennae overgrowth. Following complementation analysis and subsequent genomic sequencing, E.4.1 was identified as a novel mutant allele of GstE14, a gene involved in ecdysone biosynthesis important for the timing of developmental events. The abnormal eye and antenna phenotypes observed resulting from the loss of GstE14 suggest its role in tissue growth. 

Genetic screens in Drosophila melanogaster have long been used to identify genes found in a variety of developmental, cellular, and behavioral processes. Here we describe the characterization and mapping of a mutation identified in a conditional screen for genetic regulators of cell growth and cell division. Within a Flp/FRT system, mutant G.3.2 results in a reduction of mutant tissue and a rough eye phenotype. We find that G.3.2 maps to the gene cnk, providing further support that cnk is a critical gene in Drosophila eye development. This mutant was characterized, mapped and sequenced by undergraduate students within the Fly-CURE consortium. 

The Fly-CURE is a genetics-focused multi-institutional Course-Based Undergraduate Research Experience (CURE) that provides undergraduate students with hands-on research experiences within a course. Through the Fly-CURE, undergraduate students at diverse types of higher education institutions across the United States map and characterize novel mutants isolated from a genetic screen in Drosophila melanogaster . To date, more than 20 mutants have been studied across 20 institutions, and our scientific data have led to eleven publications with more than 500 students as authors. To evaluate the impact of the Fly-CURE experience on students, we developed and validated assessment tools to identify students’ perceived research self-efficacy, sense of belonging in science, and intent to pursue additional research opportunities. Our data, collected over three academic years and involving 14 institutions and 480 students, show gains in these metrics after completion of the Fly-CURE across all student subgroups analyzed, including comparisons of gender, academic status, racial and ethnic groups, and parents’ educational background. Importantly, our data also show differential gains in the areas of self-efficacy and interest in seeking additional research opportunities between Fly-CURE students with and without prior research experience, illustrating the positive impact of research exposure (dosage) on student outcomes. Altogether, our data indicate that the Fly-CURE experience has a significant impact on students’ efficacy with research methods, sense of belonging to the scientific research community, and interest in pursuing additional research experiences. 

An EMS-based forward genetic screen was conducted in an apoptotic null background to identify genetic aberrations that contribute to regulation of cell growth in Drosophila melanogaster. The current work maps the genomic location of one of the identified mutants, L.3.2. Genetic crosses conducted through the Fly-CURE consortium determined that the gene locus for the L.3.2 mutation is p47 on chromosome 2R. 

Mutant B.4.1 , generated via EMS mutagenesis in Drosophila melanogaster, was studied by undergraduate students participating in the Fly-CURE. After inducing genetically mosaic tissue in the adult eye, B.4.1 mutant tissue displays a robust increase in cell division and a rough appearance. Complementation mapping and sequence analysis identified a nonsense mutation in the gene CG1603 , which we named clifford ( cliff ) due to observed increases in red-pigmented mutant tissue compared to controls. cliff encodes a zinc finger-containing protein implicated in transcriptional control. RNAi knockdown of cliff similarly results in rough eyes, confirming a role for Cliff in eye development.