Role of mitochondrial DNA in human aging

Mitochondrion ◽  
2002 ◽  
Vol 2 (1-2) ◽  
pp. 27-37 ◽  
Author(s):  
Giuseppe Attardi
Keyword(s):  
Mitochondrial Dna ◽  
Human Aging

Role of mitochondrial DNA mutations in human aging: Implications for the central nervous system and muscle

1998 ◽  
Vol 43 (2) ◽  
pp. 217-223 ◽  
Author(s):  
Elizabeth J. Brierley ◽  
Margaret A. Johnson ◽  
Robert N. Lightowlers ◽  
Oliver F. W. James ◽  
Douglass M. Turnbull
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Mitochondrial Dna ◽  
Human Aging ◽  
Mitochondrial Dna Mutations ◽  
Dna Mutations ◽  
The Central Nervous System

The role of mitochondrial DNA in the cancerogenesis of cervix HPV positive women

2008 ◽  
Vol 21 (2) ◽  
pp. 85-89
Author(s):  
Alicja Warowicka ◽  
Joanna Pacholska-Bogalska ◽  
Anna Kwaśniewska ◽  
Anna Goździcka-Józefiak
Keyword(s):  
Mitochondrial Dna

Role of Mitochondrial DNA in Inflammatory Airway Diseases

2021 ◽  
pp. 1485-1499
Author(s):  
Ryan J. Snyder ◽  
Steven R. Kleeberger
Keyword(s):  
Mitochondrial Dna ◽  
Airway Diseases

scholarly journals Cytosolic Ribosomal Mutations That Abolish Accumulation of Circular Intron in the Mitochondria Without Preventing Senescence of Podospora anserina

Genetics ◽  
1997 ◽  
Vol 145 (3) ◽  
pp. 697-705 ◽  
Author(s):  
Philippe Silar ◽  
France Koll ◽  
Michèle Rossignol
Keyword(s):  
Mitochondrial Dna ◽  
Ribosomal Proteins ◽  
Podospora Anserina ◽  
Cox1 Gene ◽  
Accuracy Control ◽  
Additional Function ◽  
Mutant Proteins ◽  
Double Stranded Dna ◽  
Dna Modifications

The filamentous fungus Podospora anserina presents a degeneration syndrome called Senescence associated with mitochondrial DNA modifications. We show that mutations affecting the two different and interacting cytosolic ribosomal proteins (S7 and S19) systematically and specifically prevent the accumulation of senDNAα (a circular double-stranded DNA plasmid derived from the first intron of the mitochondrial cox1 gene or intron α) without abolishing Senescence nor affecting the accumulation of other usually observed mitochondrial DNA rearrangements. One of the mutant proteins is homologous to the Escherichia coli S4 and Saccharomyces cerevisiae S13 ribosomal proteins, known to be involved in accuracy control of cytosolic translation. The lack of accumulation of senDNAα seems to result from a nontrivial ribosomal alteration unrelated to accuracy control, indicating that S7 and S19 proteins have an additional function. The results strongly suggest that modified expression of nucleus-encoded proteins contributes to Senescence in P. anserina. These data do not fit well with some current models, which propose that intron α plays the role of the cytoplasmic and infectious Determinant of Senescence that was defined in early studies.

scholarly journals The Role of Mitochondria in Carcinogenesis

2021 ◽  
Vol 22 (10) ◽  
pp. 5100
Author(s):  
Paulina Kozakiewicz ◽  
Ludmiła Grzybowska-Szatkowska ◽  
Marzanna Ciesielka ◽  
Jolanta Rzymowska
Keyword(s):  
Prostate Cancer ◽  
Mitochondrial Dna ◽  
Nuclear Dna ◽  
Dna Polymorphisms ◽  
Gene Encoding ◽  
Dna Mutations ◽  
Nadh Ubiquinone Oxidoreductase ◽  
Gene Coi ◽  
The Impact

The mitochondria are essential for normal cell functioning. Changes in mitochondrial DNA (mtDNA) may affect the occurrence of some chronic diseases and cancer. This process is complex and not entirely understood. The assignment to a particular mitochondrial haplogroup may be a factor that either contributes to cancer development or reduces its likelihood. Mutations in mtDNA occurring via an increase in reactive oxygen species may favour the occurrence of further changes both in mitochondrial and nuclear DNA. Mitochondrial DNA mutations in postmitotic cells are not inherited, but may play a role both in initiation and progression of cancer. One of the first discovered polymorphisms associated with cancer was in the gene NADH-ubiquinone oxidoreductase chain 3 (mt-ND3) and it was typical of haplogroup N. In prostate cancer, these mutations and polymorphisms involve a gene encoding subunit I of respiratory complex IV cytochrome c oxidase subunit 1 gene (COI). At present, a growing number of studies also address the impact of mtDNA polymorphisms on prognosis in cancer patients. Some of the mitochondrial DNA polymorphisms occur in both chronic disease and cancer, for instance polymorphism G5913A characteristic of prostate cancer and hypertension.

The role of mitochondrial DNA large deletion for the development of presbycusis in Fischer 344 rats

2007 ◽  
Vol 27 (3) ◽  
pp. 370-377 ◽  
Author(s):  
Shankai Yin ◽  
Zhiping Yu ◽  
Ravi Sockalingam ◽  
Manohar Bance ◽  
Genlou Sun ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Large Deletion ◽  
Fischer 344 Rats ◽  
Fischer 344

Cytosolic and mitochondrial Hsp90 in cytokinesis, mitochondrial DNA replication, and drug action in Trypanosoma brucei

2021 ◽  
Author(s):  
Kirsten J. Meyer ◽  
Theresa A. Shapiro
Keyword(s):  
Mitochondrial Dna ◽  
Trypanosoma Brucei ◽  
Cell Biology ◽  
Drug Targets ◽  
Heat Shock Protein 90 ◽  
Cell Cycle Regulators ◽  
Hsp90 Inhibitors ◽  
African Trypanosomes ◽  
Hsp90 Activity

Trypanosoma brucei subspecies cause African sleeping sickness in humans, an infection that is commonly fatal if not treated, and available therapies are limited. Previous studies have shown that heat shock protein 90 (Hsp90) inhibitors have potent and vivid activity against bloodstream form trypanosomes. Hsp90s are phylogenetically conserved and essential catalysts that function at the crux of cell biology, where they ensure the proper folding of proteins and their assembly into multicomponent complexes. To assess the specificity of Hsp90 inhibitors and further define the role of Hsp90s in African trypanosomes, we used RNAi to knockdown cytosolic and mitochondrial Hsp90s (HSP83 and HSP84, respectively). Loss of either protein led to cell death but the phenotypes were distinctly different. Depletion of cytosolic HSP83 closely mimicked the consequences of chemically depleting Hsp90 activity with inhibitor 17-AAG. In these cells cytokinesis was severely disrupted and segregation of the kinetoplast (the massive mitochondrial DNA structure unique to this family of eukaryotic pathogens) was impaired, leading to cells with abnormal kDNA structures. Quite differently, knockdown of mitochondrial HSP84 did not impair cytokinesis but halted the initiation of new kDNA synthesis, generating cells without kDNA. These findings highlight the central role for Hsp90s in chaperoning cell cycle regulators in trypanosomes, reveal their unique function in kinetoplast replication, and reinforce their specificity and value as drug targets.

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