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Difference between revisions of "Pye 2006 Nucleic Acids Research"

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{{Publication
{{Publication
|title=Pye D, Kyriakouli DS, Taylor GA, Johnson R, Elstner M, Meunier B, Chrzanowska-Lightowlers ZMA, Taylor RW, Turnbull DM, Lightowlers RN (2006) Production of transmitochondrial cybrids containing naturally occurring pathogenic mtDNA variants. Nucleic Acids Research 34: e95
|title=Pye D, Kyriakouli DS, Taylor GA, Johnson R, Elstner M, Meunier B, Chrzanowska-Lightowlers ZMA, Taylor RW, Turnbull DM, Lightowlers RN (2006) Production of transmitochondrial cybrids containing naturally occurring pathogenic mtDNA variants. Nucleic Acids Research 34: e95
|info=[http://www.ncbi.nlm.nih.gov/pubmed/16885236 PMID: 16885236]
|authors=Pye D, Kyriakouli DS, Taylor GA, Johnson R, Elstner M, Meunier B, Chrzanowska-Lightowlers ZMA, Taylor RW, Turnbull DM, Lightowlers RN
|authors=Pye D, Kyriakouli DS, Taylor GA, Johnson R, Elstner M, Meunier B, Chrzanowska-Lightowlers ZMA, Taylor RW, Turnbull DM, Lightowlers RN
|year=2006
|year=2006
|journal=Nucleic Acids Res.
|journal=Nucleic Acids Res.
|abstract=The human mitochondrial genome (mtDNA)
|abstract=The human mitochondrial genome (mtDNA) encodes polypeptides that are critical for coupling oxidative phosphorylation. Our detailed understanding of the molecular processes that mediate mitochondrial gene expression and the structure–function relationships of the OXPHOS components could be greatly improved if we were able to transfect mitochondria and manipulate mtDNA in vivo.
encodes polypeptides that are critical for coupling
Increasing our knowledge of this process is not merely of fundamental importance, as mutations of the mitochondrial genome are known to cause a
oxidative phosphorylation. Our detailed understanding
spectrum of clinical disorders and have been implicated in more common neurodegenerative disease and the ageing process. In organellar or in vitro
of the molecular processes that mediate
reconstitution studies have identified many factors central to the mechanisms of mitochondrial gene expression, but being able to investigate the molecular
mitochondrial gene expression and the structure–
aetiology of a limited number of cell lines from patients harbouring mutated mtDNA has been enormously beneficial. In the absence of a mechanism
function relationships of the OXPHOS components
for manipulating mtDNA, a much larger pool of pathogenic mtDNA mutations would increase our knowledge of mitochondrial gene expression.
could be greatly improved if we were able to transfect
Colonic crypts from ageing individuals harbour mutated mtDNA. Here we show that by generating cytoplasts from colonocytes, standard fusion techniques
mitochondria and manipulate mtDNA in vivo.
can be used to transfer mtDNA into rapidly dividing immortalized cells and, thereby, respiratory-deficient transmitochondrial cybrids can be isolated. A simple screen identified clones that carried putative pathogenic mutations in MTRNR1, MTRNR2, MTCOI and MTND2, MTND4 and MTND6.
Increasing our knowledge of this process is not
This method can therefore be exploited to produce a library of cell lines carrying pathogenic human mtDNA for further study.
merely of fundamental importance, as mutations of
|discipline=Biomedicine
the mitochondrial genome are known to cause a
spectrum of clinical disorders and have been implicated
in more common neurodegenerative disease
and the ageing process. In organellar or in vitro
reconstitution studies have identified many factors
central to the mechanisms of mitochondrial gene
expression, but being able to investigate the molecular
aetiology of a limited number of cell lines from
patients harbouring mutated mtDNA has been
enormously beneficial. In the absence of a mechanism
for manipulating mtDNA, a much larger pool
of pathogenic mtDNA mutations would increase
our knowledge of mitochondrial gene expression.
Colonic crypts from ageing individuals harbour
mutated mtDNA. Here we show that by generating
cytoplasts from colonocytes, standard fusion techniques
can be used to transfer mtDNA into
rapidly dividing immortalized cells and, thereby,
respiratory-deficient transmitochondrial cybrids can
be isolated. A simple screen identified clones that
carried putative pathogenic mutations in MTRNR1,
MTRNR2, MTCOI and MTND2, MTND4 and MTND6.
This method can therefore be exploited to produce a
library of cell lines carrying pathogenic human
mtDNA for further study.
|info=[http://www.ncbi.nlm.nih.gov/pubmed/16885236 PMID: 16885236]
}}
}}
{{Labeling
{{Labeling
|discipline=Biomedicine
|instruments=Oxygraph-2k
|injuries=Cancer; Apoptosis; Cytochrome c, Genetic Defect; Knockdown; Overexpression
|injuries=Cancer; Apoptosis; Cytochrome c, Mitochondrial Disease; Degenerative Disease and Defect, Genetic Defect; Knockdown; Overexpression
|organism=Human
|organism=Human
|preparations=Intact Cell; Cultured; Primary
|preparations=Intact Cell; Cultured; Primary
|topics=Respiration; OXPHOS; ETS Capacity
|topics=Respiration; OXPHOS; ETS Capacity
|instruments=Oxygraph-2k
|discipline=Biomedicine
}}
}}

Revision as of 13:36, 17 November 2011

Publications in the MiPMap
Pye D, Kyriakouli DS, Taylor GA, Johnson R, Elstner M, Meunier B, Chrzanowska-Lightowlers ZMA, Taylor RW, Turnbull DM, Lightowlers RN (2006) Production of transmitochondrial cybrids containing naturally occurring pathogenic mtDNA variants. Nucleic Acids Research 34: e95

Β» PMID: 16885236

Pye D, Kyriakouli DS, Taylor GA, Johnson R, Elstner M, Meunier B, Chrzanowska-Lightowlers ZMA, Taylor RW, Turnbull DM, Lightowlers RN (2006) Nucleic Acids Res.

Abstract: The human mitochondrial genome (mtDNA) encodes polypeptides that are critical for coupling oxidative phosphorylation. Our detailed understanding of the molecular processes that mediate mitochondrial gene expression and the structure–function relationships of the OXPHOS components could be greatly improved if we were able to transfect mitochondria and manipulate mtDNA in vivo. Increasing our knowledge of this process is not merely of fundamental importance, as mutations of the mitochondrial genome are known to cause a spectrum of clinical disorders and have been implicated in more common neurodegenerative disease and the ageing process. In organellar or in vitro reconstitution studies have identified many factors central to the mechanisms of mitochondrial gene expression, but being able to investigate the molecular aetiology of a limited number of cell lines from patients harbouring mutated mtDNA has been enormously beneficial. In the absence of a mechanism for manipulating mtDNA, a much larger pool of pathogenic mtDNA mutations would increase our knowledge of mitochondrial gene expression. Colonic crypts from ageing individuals harbour mutated mtDNA. Here we show that by generating cytoplasts from colonocytes, standard fusion techniques can be used to transfer mtDNA into rapidly dividing immortalized cells and, thereby, respiratory-deficient transmitochondrial cybrids can be isolated. A simple screen identified clones that carried putative pathogenic mutations in MTRNR1, MTRNR2, MTCOI and MTND2, MTND4 and MTND6. This method can therefore be exploited to produce a library of cell lines carrying pathogenic human mtDNA for further study.


Labels:

Stress:Cancer; Apoptosis; Cytochrome c"Cancer; Apoptosis; Cytochrome c" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property., Mitochondrial Disease; Degenerative Disease and Defect"Mitochondrial Disease; Degenerative Disease and Defect" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property., Genetic Defect; Knockdown; Overexpression"Genetic Defect; Knockdown; Overexpression" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property.  Organism: Human 

Preparation: Intact Cell; Cultured; Primary"Intact Cell; Cultured; Primary" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property. 

Regulation: Respiration; OXPHOS; ETS Capacity"Respiration; OXPHOS; ETS Capacity" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property. 


HRR: Oxygraph-2k