Skip to main content
Presentation Time: 11:55-12:15
Home University: UNC-Chapel Hill
Research Mentor: Bob Duronio, Biology
Program: McNair
Research Title: Genotypic and Phenotypic Characterization of mutations in Drosophila melanogaster CG8569 which encodes a putative ortholog of the human epigenetic regulator ZMYND11

Mutations in the human ZMYND11 gene have been postulated as the cause of neurodevelopmental disorders such as autosomal dominant intellectual disability 30, the 10p15.3 microdeletion syndrome, and autism spectrum disorders. ZMYND11 encodes a nuclear protein that specifically binds variant histone H3.3 and regulates gene expression at the transcriptional level. However, the molecular mechanisms of action and the functions of ZMYND11 disrupted in human disease remain unknown. One approach to learn more about ZMYND11’s molecular behavior is studying its orthologous gene in a model organism. Our lab is investigating whether the Drosophila melanogaster CG8569 gene encodes an ortholog of human ZMYND11. The purpose of this study was to characterize a transposon insertion allele of CG8569 (CG8569EP1182) both genotypically and phenotypically. We found that the EP1182 transposon was inserted into the coding region of CG8569 and thus should disrupt its function. Nevertheless, we found that gene expression still occurs from the CG8569EP1182 mutant allele and that CG8569EP1182 mutant flies are viable, although they demonstrated reduced longevity when compared to non-mutant flies. To ask whether CG8569EP1182 mutants had neurological defects we measured several parameters of movement in developing CG8569EP1182 larvae. No statistically significant differences were observed in crawling length, crawling time, and crawling speed between mutant and wildtype flies. Together, this study shows that the mutant allele CG8569EP1182 impairs fly longevity but does not affect locomotion in larvae.