Poster Session #2

Presentation Type

Poster

Faculty Mentor’s Full Name

Ekaterina Voronina

Faculty Mentor’s Department

Division of Biological Sciences

Abstract / Artist's Statement

The activity and regulation of RNA-binding proteins (RBP) is an important topic in studies of gene expression. The regulation of RBPs includes interactions with cofactors. One cofactor that our lab has identified is DLC-1, a small protein that prompts the association of a RBP with subcellular RNA granules. Previous research on a protein, Pbp1, with similar effects in Saccharomyces cerevisiae (yeast) shows that Pbp-1 over-expression leads to growth inhibition in yeast cells due to the promotion of excessive RNA granule formation (Swisher and Parker, 2010). Due to similar effects between Pbp-1 and DLC-1, we hypothesize that DLC-1, when over-expressed, will cause growth inhibition in yeast cells. Saccharomyces cerevisiae is the model organism that we will use to investigate this question because it is cost efficient, allows for fast results, and is relevant for humans because many of the proteins present in yeast have mammalian orthologs. This hypothesis will be tested on multiple strains of yeast. Using these different strains, we will express DLC-1, two positive controls (Pab1 and Dhh1), and a negative control under the control of a galactose-inducible promotor. We will then grow the yeast on agarose plates that contain different concentrations of sugars (galactose and sucrose). We vary the concentrations of sugars in order to control the activity of the promotor, resulting in protein over-expression in higher concentrations of galactose. The yeast will then be incubated on the plates for five days. At the end of the incubation period, potential lack of cell growth on the high-galactose plate will suggest if DLC-1 over-expression does lead to inhibition of cell growth. Understanding how expression of DLC-1 is related to cell growth and RNA granule formation is important because abnormal RNA granule formation is linked to neurodegenerative diseases.

Category

Life Sciences

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Apr 27th, 3:00 PM Apr 27th, 4:00 PM

DLC-1 Over-Expression and Growth Inhibition in Saccharomyces Cerevisiae

UC South Ballroom

The activity and regulation of RNA-binding proteins (RBP) is an important topic in studies of gene expression. The regulation of RBPs includes interactions with cofactors. One cofactor that our lab has identified is DLC-1, a small protein that prompts the association of a RBP with subcellular RNA granules. Previous research on a protein, Pbp1, with similar effects in Saccharomyces cerevisiae (yeast) shows that Pbp-1 over-expression leads to growth inhibition in yeast cells due to the promotion of excessive RNA granule formation (Swisher and Parker, 2010). Due to similar effects between Pbp-1 and DLC-1, we hypothesize that DLC-1, when over-expressed, will cause growth inhibition in yeast cells. Saccharomyces cerevisiae is the model organism that we will use to investigate this question because it is cost efficient, allows for fast results, and is relevant for humans because many of the proteins present in yeast have mammalian orthologs. This hypothesis will be tested on multiple strains of yeast. Using these different strains, we will express DLC-1, two positive controls (Pab1 and Dhh1), and a negative control under the control of a galactose-inducible promotor. We will then grow the yeast on agarose plates that contain different concentrations of sugars (galactose and sucrose). We vary the concentrations of sugars in order to control the activity of the promotor, resulting in protein over-expression in higher concentrations of galactose. The yeast will then be incubated on the plates for five days. At the end of the incubation period, potential lack of cell growth on the high-galactose plate will suggest if DLC-1 over-expression does lead to inhibition of cell growth. Understanding how expression of DLC-1 is related to cell growth and RNA granule formation is important because abnormal RNA granule formation is linked to neurodegenerative diseases.