Location
University of Nevada Las Vegas, Student Union Ball Room
Start Date
6-8-2009 9:30 AM
End Date
6-8-2009 12:00 PM
Description
Climate change is fundamentally connected to animal development and survival, and the life history of an organism must be coordinated with predictable seasonal changes of the environment. Climate change affects the life cycle of plants, a major food source for insects. If photoperiod, the primary environmental queue that insects utilize to determine the proper emergence time, and food availability becomes out of sync, many populations of insects and other animals could be threatened. Understanding animal development can provide insight into this issue and could provide clues that may help the scientific community predict how insect populations may respond to climate change. During Drosophila metamorphosis, most of the larval tissues are destroyed, but the fat body is an exception. The larval fat body escapes destruction and is instead remodeled from flat, polygonal and attached sheets of cells to round, spherical and detached free-floating cells (Nelliot, et. al, 2006). It has been hypothesized that Ecdysone signaling is necessary for fat cell detachment. To test the hypothesis that Ecdysone signaling is necessary for fat cell detachment, I am using genetic techniques to create mosaic animals. These techniques will allow me to generate clones of cells that are deficient or hyperactive in certain Ecdysone signaling targets. Currently, I am trying to establish animals for the first part of a two-step cross. Next, using the FLP/FRT and the Mosaic Analysis with a Repressible Cell Marker system (MARCM), I will generate mitotic clones of cells. These clones will be comprised of small populations of cells mutant for Ecdysone signaling factors and will be surrounded by normal (wild type) cells. I predict that the populations which are deficient in Ecdysone signaling factors will not undergo fat body remodeling while the surrounding pools of wild type cells will complete the remodeling program. These two types of cells can be distinguished from each other because I will also label the Ecdysone signaling-defective cells with green fluorescent protein. The data will be procured on the Confocal Microscope in the Center for Biological Imaging.
Keywords
Climate change; Drosophila; ECDYSONE; Fat cells; Insect populations; Mosaic Analysis with a Repressible Cell Marker system (MARCM)
Disciplines
Cell and Developmental Biology | Entomology
Language
English
Role of ecdysone signaling in fat body remodeling
University of Nevada Las Vegas, Student Union Ball Room
Climate change is fundamentally connected to animal development and survival, and the life history of an organism must be coordinated with predictable seasonal changes of the environment. Climate change affects the life cycle of plants, a major food source for insects. If photoperiod, the primary environmental queue that insects utilize to determine the proper emergence time, and food availability becomes out of sync, many populations of insects and other animals could be threatened. Understanding animal development can provide insight into this issue and could provide clues that may help the scientific community predict how insect populations may respond to climate change. During Drosophila metamorphosis, most of the larval tissues are destroyed, but the fat body is an exception. The larval fat body escapes destruction and is instead remodeled from flat, polygonal and attached sheets of cells to round, spherical and detached free-floating cells (Nelliot, et. al, 2006). It has been hypothesized that Ecdysone signaling is necessary for fat cell detachment. To test the hypothesis that Ecdysone signaling is necessary for fat cell detachment, I am using genetic techniques to create mosaic animals. These techniques will allow me to generate clones of cells that are deficient or hyperactive in certain Ecdysone signaling targets. Currently, I am trying to establish animals for the first part of a two-step cross. Next, using the FLP/FRT and the Mosaic Analysis with a Repressible Cell Marker system (MARCM), I will generate mitotic clones of cells. These clones will be comprised of small populations of cells mutant for Ecdysone signaling factors and will be surrounded by normal (wild type) cells. I predict that the populations which are deficient in Ecdysone signaling factors will not undergo fat body remodeling while the surrounding pools of wild type cells will complete the remodeling program. These two types of cells can be distinguished from each other because I will also label the Ecdysone signaling-defective cells with green fluorescent protein. The data will be procured on the Confocal Microscope in the Center for Biological Imaging.
Comments
Abstract & poster