Genome Editing and the Problem of Tetraploidy in Cell Modeling of the Genetic Form of Parkinsonism
- Authors: Simonova V.V.1, Vetchinova A.S.1, Novosadova E.V.2, Khaspekov L.G.1, Illarioshkin S.N.1
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Affiliations:
- Research Center of Neurology
- Institute of Molecular Genetics
- Issue: Vol 83, No 9 (2018)
- Pages: 1040-1045
- Section: Mini-Review
- URL: https://journals.rcsi.science/0006-2979/article/view/151711
- DOI: https://doi.org/10.1134/S0006297918090055
- ID: 151711
Cite item
Abstract
The prevalent form of familial parkinsonism is caused by mutations in the LRRK2 gene encoding for the mitochondrial protein kinase. In the review, we discuss possible causes of appearance of tetraploid cells in neuronal precursors obtained from induced pluripotent stem cells from patients with the LRRK2-associated form of parkinsonism after genome editing procedure. As LRRK2 protein participates in cell proliferation and maintenance of the nuclear envelope, spindle fibers, and cytoskeleton, mutations in the LRRK2 gene can affect protein functions and lead, via various mechanisms, to the mitotic machinery disintegration and chromosomal aberration. These abnormalities can appear at different stages of fibroblast reprogramming; therefore, editing of the LRRK2 nucleotide sequence should be done during or before the reprogramming stage.
About the authors
V. V. Simonova
Research Center of Neurology
Email: snillario@gmail.com
Russian Federation, Moscow, 125367
A. S. Vetchinova
Research Center of Neurology
Email: snillario@gmail.com
Russian Federation, Moscow, 125367
E. V. Novosadova
Institute of Molecular Genetics
Email: snillario@gmail.com
Russian Federation, Moscow, 123182
L. G. Khaspekov
Research Center of Neurology
Email: snillario@gmail.com
Russian Federation, Moscow, 125367
S. N. Illarioshkin
Research Center of Neurology
Author for correspondence.
Email: snillario@gmail.com
Russian Federation, Moscow, 125367
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