Cell & Molecular Biology Graduate Group

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Kelsey Johnson, Voight lab (matriculated 2013)

Macintosh HD:Users:sundaram:Desktop:Documents:GGR stuff:Website updates 2014:Student highlights pages:Kelsey Johnson.jpgI joined the Voight Lab in June 2014 and began working on a project studying signals of positive selection in the human genome. Using data from the 1000 Genomes Project, I am identifying regions showing evidence of selective sweeps in 14 populations and quantifying the degree of sharing of sweeps between those populations. Sweeps may be shared between populations due to common ancestry, migration and gene flow, convergent evolution, or by chance. I plan to use shared sweeps to investigate the evolutionary history of these populations and potentially identify the selected adaptive variants in these regions.



Ellie Weisz, Jongens lab (matriculated 2011)

Macintosh HD:Users:sundaram:Desktop:Documents:GGR stuff:Website updates 2014:Student highlights pages:Ellie Weisz.JPGMy work in the Jongens laboratory has been focused on studying metabolism in a Drosophila model of Fragile X Syndrome (FXS). This project is particularly relevant on a translational level given that FXS is the most common heritable form of intellectual impairment and the leading genetic cause of autism. In addition to behavioral, cognitive, and physical abnormalities, the clinical literature suggests that individuals with FXS show signs of metabolic dysfunction. Despite these observations, no studies have been conducted to assess metabolism in human patients or animal models of the disease.One genetic model that has emerged as a powerful tool to study Fragile X disease pathology is Drosophila melanogaster, as flies homozygous for amorphic alleles of the Drosophila ortholog of the pathological gene in humans display behavioral, cognitive, and neuroanatomical phenotypes that are remarkably similar to those found in human patients. Recently, research from our laboratory has suggested that insulin signaling is dysregulated in the Drosophila model of FXS. Since proper regulation of insulin signaling is critical to maintain metabolic homeostasis, it is my hypothesis that metabolism is altered in the fly model of FXS. Moreover, I believe that these metabolic differences may affect behavioral and cognitive output.

Thus far I have identified striking metabolic phenotypes in Fragile X flies. Specifically, my data suggest that glycogen and triglyceride levels are drastically reduced in our model. Consequently, the Fragile X flies are much less resistant to starvation than their wild-type counterparts. These findings are particularly interesting given that my data also indicate that the Fragile X flies consume more food than wild-type flies. A similar hyperphagia phenotype has been observed in human patients, however, my studies are the first to demonstrate this in an animal model of the disease. Now that I have identified robust metabolic phenotypes in our model, my goal is to identify the molecular and genetic mechanisms underlying these changes. Further, I plan to utilize the wide array of genetic tools in Drosophila to identify the cells that are relevant to the observed metabolic changes. Finally, I plan to determine whether genetic and/or pharmacological manipulation of proteins involved in metabolism can rescue the observed behavioral, cognitive, and neuroanatomical abnormalities in our Fragile X model.

Chris Hsiung, Raj and Blobel labs (matriculated 2009)

Macintosh HD:Users:sundaram:Desktop:Documents:GGR stuff:Website updates 2014:Student highlights pages:Chris Hsiung.JPG My research is focused on understanding mechanisms of cellular memory through mitosis, a phase of the cell cycle when transcription ceases and the nucleus is disassembled in metaozoans. I examined the role of chromatin structure in memory of gene regulation during mitosis by analyzing the first genome-wide map of chromatin accessibility in mitotic cells using DNase-seq(Hsiung CC et al., Genome Research, 2014). One remarkable finding from this study is thatmaintenance of open chromatin configuration at promoters during mitosis overall exceeds that of enhancers. As a follow-up to this study, I am combining genomic approaches with single-molecule RNA FISH to study how reactivation of the silent genome after mitosis may contribute to non-genetic heterogeneity in gene expression.


Rob Plasschaert, Bartolomei lab (matriculated 2009)


My work during graduate school has focused on understanding the roles of the transcription factor CTCF during development. My first project focused on elucidating how specific sequence differences in CTCF binding sites alter CTCF's recruitment and function during mouse embryonic stem cell differentiation (Plasschaert et al., 2013). My current project hopes to explain CTCF's role in expression of Grb10, an imprinted gene which switches from maternal to paternal expression during neuronal commitment through an unclear mechanism. To study this question, I have adopted an in vitro differentiation system of generating motor neurons from mouse embryonic stem cells. This system successfully mimics the switch in maternal to paternal Grb10 expression seen in vivo during neuronal development, enabling the study of Grb10 regulation in an amenable cell culture system.