Event Title

Manipulating the Caenorhabditis elegans Gene daf-16 to Understand Longevity

Presenter Information

Kyle Manning, Biology

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

Caenorhabditis elegans are effective model organisms for gaining insights into human health because they share approximately 46% of human genes. C. elegans contain the gene daf-16, which is orthologous to the human FOXO genes. FOXO genes activate many different pathways by turning genes on in response to stress. These pathways are involved in control of cell growth, apoptosis, DNA repair, and oxidative stress. Thus, when these genes are activated, the system amplifies the activity of these protective mechanisms, which enables prolonged lifespan. Using RNAi, the daf-16 gene can be silenced by using a specific RNAi feeding vector. With daf-16 knocked down, the system loses its ability to activate these protective mechanisms. An acute juglone sensitivity assay will be used to verify the effectiveness of the RNAi mechanism and determine the vulnerability of the mutated worms to oxidative stress. Thus, when the worms are stressed, they are less able to cope with the stress, and are expected to die much faster than the control worm. This experiment will show the importance of these pathways to prolonged lifespan.

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

Manipulating the Caenorhabditis elegans Gene daf-16 to Understand Longevity

Hartman Union Building Courtroom

Caenorhabditis elegans are effective model organisms for gaining insights into human health because they share approximately 46% of human genes. C. elegans contain the gene daf-16, which is orthologous to the human FOXO genes. FOXO genes activate many different pathways by turning genes on in response to stress. These pathways are involved in control of cell growth, apoptosis, DNA repair, and oxidative stress. Thus, when these genes are activated, the system amplifies the activity of these protective mechanisms, which enables prolonged lifespan. Using RNAi, the daf-16 gene can be silenced by using a specific RNAi feeding vector. With daf-16 knocked down, the system loses its ability to activate these protective mechanisms. An acute juglone sensitivity assay will be used to verify the effectiveness of the RNAi mechanism and determine the vulnerability of the mutated worms to oxidative stress. Thus, when the worms are stressed, they are less able to cope with the stress, and are expected to die much faster than the control worm. This experiment will show the importance of these pathways to prolonged lifespan.