Presenter Information

Anna Justis, University of Wyoming

Department

Department of Molecular Biology

First Advisor

Dr. David Fay

Description

The ethanol and stress response element (ESRE) network in Caenorhabditis elegans regulates stress - induced gene expression. The ESRE network is highly c onserved and is involved in responding to a variety of environmental stresses. The ESRE motif is predicted to be the binding site of an unknown transcription factor, termed the ESRE - binding protein (EBP). This project aims to identify the EBP and other p otential ESRE regulatory molecules using a combined approach of RNAi and mutational genetic screens. The RNAi screen consisted of knocking down known transcription factors and signaling molecules in C. elegans and looking for a subsequent decrease in an E SRE - dependent fluorescence reporter signal, indicating interference with the ESRE stress response. The mutational screen consisted of inducing random mutations in the genome and looking for a change in the expression of ESRE - dependent fluorescence reporte rs. This screen resulted in gain - of - function mutations that cause constitutive expression of ESRE genes as well as loss - of - function mutations that cause a reduced ESRE response after induction of stress. Further analysis of the selected candidates may rev eal the identity of members of the ESRE regulatory network.

Comments

Oral Presentation, UW Honors Program

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Elucidating the ESRE Stress Response Network

The ethanol and stress response element (ESRE) network in Caenorhabditis elegans regulates stress - induced gene expression. The ESRE network is highly c onserved and is involved in responding to a variety of environmental stresses. The ESRE motif is predicted to be the binding site of an unknown transcription factor, termed the ESRE - binding protein (EBP). This project aims to identify the EBP and other p otential ESRE regulatory molecules using a combined approach of RNAi and mutational genetic screens. The RNAi screen consisted of knocking down known transcription factors and signaling molecules in C. elegans and looking for a subsequent decrease in an E SRE - dependent fluorescence reporter signal, indicating interference with the ESRE stress response. The mutational screen consisted of inducing random mutations in the genome and looking for a change in the expression of ESRE - dependent fluorescence reporte rs. This screen resulted in gain - of - function mutations that cause constitutive expression of ESRE genes as well as loss - of - function mutations that cause a reduced ESRE response after induction of stress. Further analysis of the selected candidates may rev eal the identity of members of the ESRE regulatory network.