Event Title

Gonad Dysgenesis Linked to the ODG1 Gene in C. elegans

Faculty Sponsor(s)

Susan Swope

Location

Hartman Union Building Courtroom

Presentation Type

Event

Start Date

5-3-2018 2:00 PM

End Date

5-3-2018 3:00 PM

Abstract

After researching genes that are shared between humans and C. elegans, we decided to take a closer look at the ODG1gene. The protein associated with this gene is the follicle stimulating hormone receptor (FSHR). FSHR is a G-protein coupled receptor and is necessary for the hormonal functioning of follicle stimulating hormone (FSH).. Mutations in this gene in humans can cause ovarian dysgenesis type 1 or ovarian hyperstimulation syndrome. The purpose of this project is to isolate a specific gene sequence and produce a feeding vector for C. elegans in order to silence the ODG1gene. DNA isolation from C. elegans provided a template for PCR amplification and by using e-RNAi blast, the primers were calculated for FSHR to use for PCR. The product of the was inserted into the vector and used to make an RNAi feeding strain of E. coli . We expect that silencing of the gene will show signs of abnormal reproduction. To test this hypothesis, we will study C. elegans carefully and observe their lifecycles. If reproduction is scarce, we can conclude that the RNAi treatment has successfully prevented synthesis of the FSHR protein, and document the observed phenotype

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May 3rd, 2:00 PM May 3rd, 3:00 PM

Gonad Dysgenesis Linked to the ODG1 Gene in C. elegans

Hartman Union Building Courtroom

After researching genes that are shared between humans and C. elegans, we decided to take a closer look at the ODG1gene. The protein associated with this gene is the follicle stimulating hormone receptor (FSHR). FSHR is a G-protein coupled receptor and is necessary for the hormonal functioning of follicle stimulating hormone (FSH).. Mutations in this gene in humans can cause ovarian dysgenesis type 1 or ovarian hyperstimulation syndrome. The purpose of this project is to isolate a specific gene sequence and produce a feeding vector for C. elegans in order to silence the ODG1gene. DNA isolation from C. elegans provided a template for PCR amplification and by using e-RNAi blast, the primers were calculated for FSHR to use for PCR. The product of the was inserted into the vector and used to make an RNAi feeding strain of E. coli . We expect that silencing of the gene will show signs of abnormal reproduction. To test this hypothesis, we will study C. elegans carefully and observe their lifecycles. If reproduction is scarce, we can conclude that the RNAi treatment has successfully prevented synthesis of the FSHR protein, and document the observed phenotype