Danielle Herrig and Patrick Lansdon to present at Student Seminar 7/11/2016

Danielle’s Abstract

Speciation Genetics in Drosophila: Insights from Male and Female Transcriptomes

Population genetic models predict that the X chromosome will evolve at a faster rate than autosomes (i.e., faster-X evolution). The basis for faster-X evolution is that recessive genes located on the X chromosome can be exposed in males while these genes are hidden if located on the autosomes. Evaluations of protein-coding sequences have indeed shown mixed results with some studies showing an excess of divergence on the X chromosome compared to autosomes, particularly in genes expressed higher in males than in females (i.e., male-biased genes). In addition, whole-genome analyses of gene expression in Drosophila yakuba and D. santomea males indicate that X-linked genes are more differentially expressed between species (i.e., faster-X evolution of gene expression) than autosomal genes. This trend is once again strongest for male-biased genes. However, these studies utilized only males and were therefore limited in their expression profiles. Here, we investigate the whole-genome profiles of D. yakuba and D. santomea males and females to determine the relative rates of evolution for all gene classes. In addition, we explore the implications of sex chromosome inheritance on autosomal gene expression in the hybrids of these species.

Patrick’s Abstract


It is widely recognized that mutations in genes encoding voltage-gated sodium (Nav) channels contribute to the etiology underlying various seizure disorders. Shudderer (Shu), a gain-of-function mutant for the Drosophila Nav channel gene, exhibits neuronal hyperexcitability and seizure-like behavioral defects, including spontaneous jerking and heat-induced convulsion. Results of microarray analyses indicated that Shu mutants have an increased innate immune response and reduced insulin signaling. Because the endogenous gut microbiota has a substantial impact on the host immune system and insulin-mediated metabolic regulation, we hypothesized that the microbiome plays a role in Shu phenotypes. Intriguingly, removing the gut microbiota of Shu and wild-type (WT) flies using antibiotic-containing or sterile food significantly suppressed Shu behavioral phenotypes while having no effect on WT behavior. Culturing homogenized guts dissected from Shu and WT flies on MRS agar revealed drastic differences in the number of culturable bacteria. Further, we performed high-throughput sequencing of the bacterial 16S ribosomal RNA gene which revealed species-specific differences in the gut microbiome of Shu and WT flies. Because neurological disorders and changes in the microbiota can individually increase oxidative stress in an organism, we examined the antioxidant response in the guts of Shu and WT flies using a GFP reporter, (GST-D-GFP). GST-D-GFP expression was altered in Shu and WT flies fed antibiotics, suggesting a potential involvement of oxidative stress in the antibiotic-dependent rescue of seizure-like behavior. Additional experiments will determine ROS levels in Shu and WT flies and are expected to yield a better understanding of the role of the microbiome in the context of seizure disorders.


Posted on July 11, 2016, in Student Seminar. Bookmark the permalink. Leave a comment.

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