Effects of ERAD E3 ligase mutations on C. elegans food seeking behavior
Research Mentor(s)
Dahlberg, Lina
Description
Endoplasmic Reticulum Associated Degradation (ERAD) is a cellular process that prevents protein aggregation by tagging misfolded proteins with ubiquitin at the endoplasmic reticulum (ER), marking them for destruction (figure 1) (7,6,5). E3 ubiquitin ligases participate in the ubiquination process of target proteins during ERAD (figure 1) (7,6,5). Protein aggregation is important to study because it is seen in neurodegenerative disorders such as Alzheimer’s and Parkinson’s disease (7). In order to research how ERAD works to prevent protein aggregation, a model protein, GLR-1, is used for this research. GLR-1 is required for food seeking behaviors in the microscopic worm, C. elegans (3). In order to understand what interactions GLR-1 may have with each of the E3 ligases that are involved in the ERAD pathway, the food seeking behavior of three different C. elegans strains that each have one mutated, non-functional E3 ligase, hrdl-1, hrd-1 and marc-6, were tested and compared.
Document Type
Event
Start Date
17-5-2018 9:00 AM
End Date
17-5-2018 12:00 PM
Department
Biology
Genre/Form
student projects, posters
Subjects – Topical (LCSH)
Ubiquitin; Protein folding; Proteins--Metabolism; Proteins--Pathophysiology
Type
Image
Rights
Copying of this document in whole or in part is allowable only for scholarly purposes. It is understood, however, that any copying or publication of this documentation for commercial purposes, or for financial gain, shall not be allowed without the author's written permission.
Language
English
Format
application/pdf
Effects of ERAD E3 ligase mutations on C. elegans food seeking behavior
Endoplasmic Reticulum Associated Degradation (ERAD) is a cellular process that prevents protein aggregation by tagging misfolded proteins with ubiquitin at the endoplasmic reticulum (ER), marking them for destruction (figure 1) (7,6,5). E3 ubiquitin ligases participate in the ubiquination process of target proteins during ERAD (figure 1) (7,6,5). Protein aggregation is important to study because it is seen in neurodegenerative disorders such as Alzheimer’s and Parkinson’s disease (7). In order to research how ERAD works to prevent protein aggregation, a model protein, GLR-1, is used for this research. GLR-1 is required for food seeking behaviors in the microscopic worm, C. elegans (3). In order to understand what interactions GLR-1 may have with each of the E3 ligases that are involved in the ERAD pathway, the food seeking behavior of three different C. elegans strains that each have one mutated, non-functional E3 ligase, hrdl-1, hrd-1 and marc-6, were tested and compared.