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Mitochondrial dysfunction in humans by cyto-nuclear incompatibility

Lusseveld, J.H. and Beukeboom, L.W. (2016) Mitochondrial dysfunction in humans by cyto-nuclear incompatibility. Bachelor's Thesis, Biology.

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Abstract

Mitochondria provide energy for the cell by using sugars and lipids and converting stored energy in the form of a proton gradient into usable ATP. Mitochondria are also responsible for calcium signalling, cell metabolism regulation, steroid synthesis and apoptosis. Mitochondrial proteins are mostly encoded by nuclear DNA (nDNA), but mitochondria also have their own DNA (mtDNA). This mtDNA is 17 kb long circular double stranded DNA, and has a high mutation rate because of its proximity to oxidative phosphorylation in mitochondria. Different mtDNA genomes exist within the human population, this is caused by mutations in mtDNA and subsequent mutations in nDNA over the course of generations that reverse the pathogenic effect. These different mtDNA genomes are called haplotypes and suggested to be linked to several diseases, for example Leber’s hereditary optic neuropathy (LHON). Pathogenic point mutations can be transferred maternally and transfer mitochondrial disease to next generations. Treating or preventing mitochondrial disease is very difficult because many mechanisms are not yet fully understood. Examples are the mtDNA ‘bottleneck’ and mitochondrial segregation in cell division. There are currently several therapies to prevent mitochondrial disease, all of which involve using a donor oocyte with ‘healthy mtDNA’. There are however still many uncertainties using these techniques and more knowledge about mitochondrial evolution and interaction with nDNA can improve these therapies.

Item Type: Thesis (Bachelor's Thesis)
Degree programme: Biology
Thesis type: Bachelor's Thesis
Language: English
Date Deposited: 15 Feb 2018 08:10
Last Modified: 15 Feb 2018 08:10
URI: http://fse.studenttheses.ub.rug.nl/id/eprint/13647

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