Presentation Type

Poster - Campus Access Only

Abstract

The regulation of RNA-binding protein (RBP) activity in cells is a central question in gene expression studies. One important RBP is GLD-1; this particular protein prompts the germ cell switch from mitotic proliferation to differentiation thus acting as a tumor suppressor. Previous research in our lab identified a small protein, DLC-1, as a cofactor of an RBP FBF-2. We hypothesized that DLC-1 may also promote the RNA regulatory function of GLD-1 because DLC-1 interacts with many cellular proteins. Caenorhabditis elegans (C. elegans) is the model organism that we use to investigate this interaction because many of the proteins present in C. elegans are also present in humans. This protein conservation allows us to utilize the benefits of studying C. elegans, such as cost efficiency and quick results, while being able to maintain human relevance. We tested our hypothesis on several strains of C. elegans that express fluorescent reporter proteins under control of GLD-1. These reporters are normally repressed by GLD-1 during differentiation. When we knockdown DLC-1 we can see how it affects the reporter’s repression. Fluorescence microscopy revealed that the genetic knockdown of DLC-1 resulted in derepression of a subset of the reporters during differentiation. Our hypothesis that DLC-1 promotes GLD-1 functions is supported by the derepression of the reporters when DLC-1 is knocked down because loss of DLC-1 results in loss of GLD-1 function. Identifying this relationship between DLC-1 and GLD-1 is important for understanding stem cell balance. When the stem cell balance between mitotic proliferation and differentiation is altered, it can result in serious consequences such as unchecked cell proliferation, tumor formations, infertility, and cancer. Understanding the mechanism(s) by which DLC-1 promotes GLD-1 would be extremely relevant to advancing our understanding of certain human diseases like cancer.

Category

Health and Medical Science

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Apr 28th, 11:00 AM Apr 28th, 12:00 PM

Investigating the interaction of DLC-1 and GLD-1 in regulation of gene expression.

UC South Ballroom

The regulation of RNA-binding protein (RBP) activity in cells is a central question in gene expression studies. One important RBP is GLD-1; this particular protein prompts the germ cell switch from mitotic proliferation to differentiation thus acting as a tumor suppressor. Previous research in our lab identified a small protein, DLC-1, as a cofactor of an RBP FBF-2. We hypothesized that DLC-1 may also promote the RNA regulatory function of GLD-1 because DLC-1 interacts with many cellular proteins. Caenorhabditis elegans (C. elegans) is the model organism that we use to investigate this interaction because many of the proteins present in C. elegans are also present in humans. This protein conservation allows us to utilize the benefits of studying C. elegans, such as cost efficiency and quick results, while being able to maintain human relevance. We tested our hypothesis on several strains of C. elegans that express fluorescent reporter proteins under control of GLD-1. These reporters are normally repressed by GLD-1 during differentiation. When we knockdown DLC-1 we can see how it affects the reporter’s repression. Fluorescence microscopy revealed that the genetic knockdown of DLC-1 resulted in derepression of a subset of the reporters during differentiation. Our hypothesis that DLC-1 promotes GLD-1 functions is supported by the derepression of the reporters when DLC-1 is knocked down because loss of DLC-1 results in loss of GLD-1 function. Identifying this relationship between DLC-1 and GLD-1 is important for understanding stem cell balance. When the stem cell balance between mitotic proliferation and differentiation is altered, it can result in serious consequences such as unchecked cell proliferation, tumor formations, infertility, and cancer. Understanding the mechanism(s) by which DLC-1 promotes GLD-1 would be extremely relevant to advancing our understanding of certain human diseases like cancer.