Publications by authors named "N Verechshagina"
Article Synopsis
- Mitochondrial DNA defects are linked to neuromuscular and neurodegenerative diseases, but current treatment methods are ineffective due to the presence of mutant DNA alongside normal DNA.
- The severity of these diseases correlates with the ratio of mutant to normal mitochondrial DNA, suggesting that shifting this balance towards normal DNA could mitigate symptoms.
- The CRISPR/Cas9 system shows promise for this purpose, as modifications to guide RNA (gRNA) allow mitochondrial integration without losing functionality, making it easier and more efficient than previous gene therapy approaches.
Many mitochondrial genes have been transferred to the nucleus in course of evolution. The products of expression of these genes, being still necessary for organelle function, are imported there from the cytosol. Molecular mechanisms of protein import are studied much deeper than those of nucleic acids.
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Mitochondrial DNA A DNA Mapp Seq Anal
March 2019
ATP and other metabolites, which are necessary for the development, maintenance, and functioning of bodily cells are all synthesized in the mitochondria. Multiple copies of the genome, present within the mitochondria, together with its maternal inheritance, determine the clinical manifestation and spreading of mutations in mitochondrial DNA (mtDNA). The main obstacle in the way of thorough understanding of mitochondrial biology and the development of gene therapy methods for mitochondrial diseases is the absence of systems that allow to directly change mtDNA sequence.
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