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dc.contributor.authorSrivastava, Amit Kumar
dc.creatorSrivastava, Amit Kumaren_US
dc.date.accessioned2011-10-19T18:46:39Z
dc.date.available2011-10-19T18:46:39Z
dc.date.issued2010-05
dc.identifier.citationSrivastava, Amit Kumar. (2010). Dmiro Interaction Screen (Bachelor's thesis, University of Arizona, Tucson, USA).
dc.identifier.urihttp://hdl.handle.net/10150/146040
dc.description.abstractMitochondria and their role in ATP production are the backbone of energetic demands in living organisms. This demand is especially seen in neurons, brain cells with specialized processes like action potential propagation and neurotransmitter release. Neuronal high-energy demands make mitochondrial transport essential for neuronal function and survival. Although the importance of mitochondrial atypical Rho-like GTPase (Miro) for mitochondrial transport is known, many questions remain. The following genomic screen aimed to identify other proteins involved in the Miro pathway, testing for genetic interactions between heterozygous dmiro null mutations and heterozygous deficiencies (deletions) covering approximately 85% of the Drosophila genome. Using live time-lapse imaging of GFP-labeled mitochondria in motor axons of larval Drosophila nerves, mitochondrial flux, the number of mitochondria moving per minute, was examined for deficiencies either enhancing or suppressing the mitochondrial flux phenotype of heterozygous dmiro null mutations, suggesting interaction with the Miro signaling pathway. Significant differences from control were defined as "candidate deficiencies" and subjected to retests; these regions were narrowed down to "map" the modifier mutations to individual genes. A total of 38 deficiencies were identified to interact with Miro. Of these, 7 deficiencies were further mapped and 14 genes were identified as strong candidates for Mirointeracting genes.
dc.language.isoenen_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/
dc.titleDmiro Interaction Screenen_US
dc.typetexten_US
dc.typeElectronic Thesisen_US
thesis.degree.grantorUniversity of Arizonaen_US
thesis.degree.levelbachelorsen_US
thesis.degree.disciplineHonors Collegeen_US
thesis.degree.disciplineMolecular and Cellular Biologyen_US
thesis.degree.nameB.S.en_US
refterms.dateFOA2018-08-22T09:17:54Z
html.description.abstractMitochondria and their role in ATP production are the backbone of energetic demands in living organisms. This demand is especially seen in neurons, brain cells with specialized processes like action potential propagation and neurotransmitter release. Neuronal high-energy demands make mitochondrial transport essential for neuronal function and survival. Although the importance of mitochondrial atypical Rho-like GTPase (Miro) for mitochondrial transport is known, many questions remain. The following genomic screen aimed to identify other proteins involved in the Miro pathway, testing for genetic interactions between heterozygous dmiro null mutations and heterozygous deficiencies (deletions) covering approximately 85% of the Drosophila genome. Using live time-lapse imaging of GFP-labeled mitochondria in motor axons of larval Drosophila nerves, mitochondrial flux, the number of mitochondria moving per minute, was examined for deficiencies either enhancing or suppressing the mitochondrial flux phenotype of heterozygous dmiro null mutations, suggesting interaction with the Miro signaling pathway. Significant differences from control were defined as "candidate deficiencies" and subjected to retests; these regions were narrowed down to "map" the modifier mutations to individual genes. A total of 38 deficiencies were identified to interact with Miro. Of these, 7 deficiencies were further mapped and 14 genes were identified as strong candidates for Mirointeracting genes.


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