Genetic Suppressors of mrp-5 Lethality in C. elegans

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dc.contributor.advisorHamza, Iqbalen_US
dc.contributor.authorBeardsley, Simonen_US
dc.contributor.departmentAnimal Sciencesen_US
dc.contributor.publisherDigital Repository at the University of Marylanden_US
dc.contributor.publisherUniversity of Maryland (College Park, Md.)en_US
dc.date.accessioned2016-06-22T06:23:06Z
dc.date.available2016-06-22T06:23:06Z
dc.date.issued2016en_US
dc.description.abstractHeme is an essential cofactor in numerous proteins, but is also cytotoxic. Thus, directed pathways must exist for regulating heme homeostasis. C. elegans is a powerful genetic animal model for elucidating these pathways because it is a heme auxotroph. Worms acquire dietary heme though HRG-1-related importers, and intestinal export was demonstrated to be mediated by the ABC transporter MRP-5. Loss of mrp-5 results in embryonic lethality. Although heme transporters have been identified, there are significant gaps in our understanding for the heme trafficking beyond HRG-1 and MRP-5. To identify additional components, we conducted a forward genetic screen utilizing the null allele mrp-5(ok2067). Screening of 160,000 haploid genomes yielded thirty-two mrp-5(ok2067) suppressor mutants. Deep-sequencing variant analysis revealed three of the suppressors subunits of adapter protein complex 3 (AP-3). We now seek to identify mechanisms for how adaptor protein deficiencies bypass a defect in MRP-5-mediated heme export.en_US
dc.identifierhttps://doi.org/10.13016/M26R4M
dc.identifier.urihttp://hdl.handle.net/1903/18437
dc.language.isoenen_US
dc.subject.pqcontrolledGeneticsen_US
dc.subject.pqcontrolledMolecular biologyen_US
dc.subject.pqcontrolledBiologyen_US
dc.subject.pquncontrolledc. elegansen_US
dc.subject.pquncontrolledhemeen_US
dc.subject.pquncontrolledmicronutrient traffickingen_US
dc.subject.pquncontrolledmrp-5en_US
dc.subject.pquncontrolledsuppressoren_US
dc.titleGenetic Suppressors of mrp-5 Lethality in C. elegansen_US
dc.typeThesisen_US

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