Presentation Type

Poster

Abstract

Genomic imprinting is a mechanism that regulates the expression of one copy of a gene differently from the other. Disruption of genomic imprinting has been linked to growth-related disease and tumor formation in humans, as well as growth effects in hybrids between many mammal species. Here we use hybrid dwarf hamsters as a model to link the evolution of gene regulation to development in mammals. Previous work has identified growth-related genes that show abnormal imprinting in placental tissues of dwarf hamsters, and whose expression levels are significantly lower in hybrids than in either parent species. These observations have led to the hypothesis that these genes are under-expressed growth repressors, however, the underlying mechanism of this remains unknown. This study examines whether disruption of DNA methylation, a common form of imprinting, could be causing the under-expression of these genes. Genes tend to be activated when not methylated, and silenced when highly methylated. I have identified candidate promoter regions, regulatory regions upstream of a gene, of a subset of these miss-expressed genes to test for differential methylation patterns between the overgrown hybrids and the parent species. I performed bisulfite sequencing on these gene regions, which allows me to quantify patterns of differential methylation. I am using these data to test the hypothesis that changes in DNA methylation underlie the disruption of gene expression in overgrown hybrids. The results will allow us to connect specific regulatory mechanisms to these striking phenotypes, giving us an increased understanding of how the evolution of gene regulation contributes to speciation and diverse growth-related diseases in humans.

Category

Life Sciences

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Apr 28th, 3:00 PM Apr 28th, 4:00 PM

Disruption of Imprinting and Abnormal Growth in Hybrids

UC South Ballroom

Genomic imprinting is a mechanism that regulates the expression of one copy of a gene differently from the other. Disruption of genomic imprinting has been linked to growth-related disease and tumor formation in humans, as well as growth effects in hybrids between many mammal species. Here we use hybrid dwarf hamsters as a model to link the evolution of gene regulation to development in mammals. Previous work has identified growth-related genes that show abnormal imprinting in placental tissues of dwarf hamsters, and whose expression levels are significantly lower in hybrids than in either parent species. These observations have led to the hypothesis that these genes are under-expressed growth repressors, however, the underlying mechanism of this remains unknown. This study examines whether disruption of DNA methylation, a common form of imprinting, could be causing the under-expression of these genes. Genes tend to be activated when not methylated, and silenced when highly methylated. I have identified candidate promoter regions, regulatory regions upstream of a gene, of a subset of these miss-expressed genes to test for differential methylation patterns between the overgrown hybrids and the parent species. I performed bisulfite sequencing on these gene regions, which allows me to quantify patterns of differential methylation. I am using these data to test the hypothesis that changes in DNA methylation underlie the disruption of gene expression in overgrown hybrids. The results will allow us to connect specific regulatory mechanisms to these striking phenotypes, giving us an increased understanding of how the evolution of gene regulation contributes to speciation and diverse growth-related diseases in humans.