Defects in multiple complexes of the respiratory chain are present in ageing human colonic crypts

Mitochondrial DNA (mtDNA) mutations accumulate in a number of ageing tissues and are proposed to play a role in the ageing process. We have previously shown that colonic crypt stem cells accumulate somatic mtDNA point mutations during ageing. These mtDNA mutations result in the loss of the activity...

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Published in	Experimental gerontology Vol. 45; no. 7-8; pp. 573 - 579
Main Authors	Greaves, Laura C., Barron, Martin J., Plusa, Stefan, Kirkwood, Thomas B., Mathers, John C., Taylor, Robert W., Turnbull, Doug M.
Format	Journal Article
Language	English
Published	England Elsevier Inc 01.08.2010 Elsevier Science
Subjects	Adolescent Adult Aged Aged, 80 and over Ageing Aging - genetics Aging - metabolism Aging - pathology Amino Acid Substitution Base Sequence Colon Colon - anatomy & histology Colon - metabolism DNA Mutational Analysis DNA, Mitochondrial - genetics Electron Transport - genetics Electron Transport - physiology Electron Transport Complex I - metabolism Electron Transport Complex II - metabolism Electron Transport Complex III - metabolism Electron Transport Complex IV - metabolism Genome, Mitochondrial Humans Immunohistochemistry Intestinal Mucosa - anatomy & histology Intestinal Mucosa - metabolism Middle Aged Mitochondria Mitochondrial Diseases - genetics Mitochondrial Diseases - metabolism mtDNA Mutation Point Mutation Respiratory chain Young Adult Mitochondria Respiratory chain Colon Mutation mtDNA Ageing
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ISSN	0531-5565 1873-6815 1873-6815
DOI	10.1016/j.exger.2010.01.013

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Abstract	Mitochondrial DNA (mtDNA) mutations accumulate in a number of ageing tissues and are proposed to play a role in the ageing process. We have previously shown that colonic crypt stem cells accumulate somatic mtDNA point mutations during ageing. These mtDNA mutations result in the loss of the activity of complex IV (cytochrome c oxidase (COX)) of the respiratory chain in the stem cells and their progeny, producing colonic crypts which are entirely COX deficient. However it is not known whether the other complexes of the respiratory chain are similarly affected during ageing. Here we have used antibodies to individual subunits of complexes I–IV to investigate their expression in the colonic epithelium from human subjects aged 18–84. We show that in ∼50% of crypts with any form of respiratory chain deficiency, decreased expression of subunits of multiple complexes is observed. Furthermore we have sequenced the entire mitochondrial genome of a number of cells with multiple complex defects and have found a wide variety of point mutations in these cells affecting a number of different protein encoding and RNA encoding genes. Finally we discuss the possible mechanisms by which multiple respiratory chain complex defects may occur in these cells.
AbstractList	Mitochondrial DNA (mtDNA) mutations accumulate in a number of ageing tissues and are proposed to play a role in the ageing process. We have previously shown that colonic crypt stem cells accumulate somatic mtDNA point mutations during ageing. These mtDNA mutations result in the loss of the activity of complex IV (cytochrome c oxidase (COX)) of the respiratory chain in the stem cells and their progeny, producing colonic crypts which are entirely COX deficient. However it is not known whether the other complexes of the respiratory chain are similarly affected during ageing. Here we have used antibodies to individual subunits of complexes I-IV to investigate their expression in the colonic epithelium from human subjects aged 18-84. We show that in approximately 50% of crypts with any form of respiratory chain deficiency, decreased expression of subunits of multiple complexes is observed. Furthermore we have sequenced the entire mitochondrial genome of a number of cells with multiple complex defects and have found a wide variety of point mutations in these cells affecting a number of different protein encoding and RNA encoding genes. Finally we discuss the possible mechanisms by which multiple respiratory chain complex defects may occur in these cells. Mitochondrial DNA (mtDNA) mutations accumulate in a number of ageing tissues and are proposed to play a role in the ageing process. We have previously shown that colonic crypt stem cells accumulate somatic mtDNA point mutations during ageing. These mtDNA mutations result in the loss of the activity of complex IV (cytochrome c oxidase (COX)) of the respiratory chain in the stem cells and their progeny, producing colonic crypts which are entirely COX deficient. However it is not known whether the other complexes of the respiratory chain are similarly affected during ageing. Here we have used antibodies to individual subunits of complexes I–IV to investigate their expression in the colonic epithelium from human subjects aged 18–84. We show that in ∼50% of crypts with any form of respiratory chain deficiency, decreased expression of subunits of multiple complexes is observed. Furthermore we have sequenced the entire mitochondrial genome of a number of cells with multiple complex defects and have found a wide variety of point mutations in these cells affecting a number of different protein encoding and RNA encoding genes. Finally we discuss the possible mechanisms by which multiple respiratory chain complex defects may occur in these cells. Mitochondrial DNA (mtDNA) mutations accumulate in a number of ageing tissues and are proposed to play a role in the ageing process. We have previously shown that colonic crypt stem cells accumulate somatic mtDNA point mutations during ageing. These mtDNA mutations result in the loss of the activity of complex IV (cytochrome c oxidase (COX)) of the respiratory chain in the stem cells and their progeny, producing colonic crypts which are entirely COX deficient. However it is not known whether the other complexes of the respiratory chain are similarly affected during ageing. Here we have used antibodies to individual subunits of complexes I-IV to investigate their expression in the colonic epithelium from human subjects aged 18-84. We show that in approximately 50% of crypts with any form of respiratory chain deficiency, decreased expression of subunits of multiple complexes is observed. Furthermore we have sequenced the entire mitochondrial genome of a number of cells with multiple complex defects and have found a wide variety of point mutations in these cells affecting a number of different protein encoding and RNA encoding genes. Finally we discuss the possible mechanisms by which multiple respiratory chain complex defects may occur in these cells.Mitochondrial DNA (mtDNA) mutations accumulate in a number of ageing tissues and are proposed to play a role in the ageing process. We have previously shown that colonic crypt stem cells accumulate somatic mtDNA point mutations during ageing. These mtDNA mutations result in the loss of the activity of complex IV (cytochrome c oxidase (COX)) of the respiratory chain in the stem cells and their progeny, producing colonic crypts which are entirely COX deficient. However it is not known whether the other complexes of the respiratory chain are similarly affected during ageing. Here we have used antibodies to individual subunits of complexes I-IV to investigate their expression in the colonic epithelium from human subjects aged 18-84. We show that in approximately 50% of crypts with any form of respiratory chain deficiency, decreased expression of subunits of multiple complexes is observed. Furthermore we have sequenced the entire mitochondrial genome of a number of cells with multiple complex defects and have found a wide variety of point mutations in these cells affecting a number of different protein encoding and RNA encoding genes. Finally we discuss the possible mechanisms by which multiple respiratory chain complex defects may occur in these cells. Mitochondrial DNA (mtDNA) mutations accumulate in a number of ageing tissues and are proposed to play a role in the ageing process. We have previously shown that colonic crypt stem cells accumulate somatic mtDNA point mutations during ageing. These mtDNA mutations result in the loss of the activity of complex IV (cytochrome c oxidase (COX)) of the respiratory chain in the stem cells and their progeny, producing colonic crypts which are entirely COX deficient. However it is not known whether the other complexes of the respiratory chain are similarly affected during ageing. Here we have used antibodies to individual subunits of complexes I–IV to investigate their expression in the colonic epithelium from human subjects aged 18–84. We show that in ∼50% of crypts with any form of respiratory chain deficiency, decreased expression of subunits of multiple complexes is observed. Furthermore we have sequenced the entire mitochondrial genome of a number of cells with multiple complex defects and have found a wide variety of point mutations in these cells affecting a number of different protein encoding and RNA encoding genes. Finally we discuss the possible mechanisms by which multiple respiratory chain complex defects may occur in these cells.
Author	Barron, Martin J. Turnbull, Doug M. Kirkwood, Thomas B. Taylor, Robert W. Mathers, John C. Greaves, Laura C. Plusa, Stefan
AuthorAffiliation	b Department of Surgery, Medical School, University of Newcastle upon Tyne, Framlington Place, Newcastle upon Tyne, NE2 4HH, UK a Mitochondrial Research Group, Institute for Ageing and Health, Medical School, University of Newcastle upon Tyne, Framlington Place, Newcastle upon Tyne, NE2 4HH, UK c Institute for Ageing and Health, Henry Wellcome Laboratory for Biogerontology Research, Newcastle University, Campus for Ageing and Vitality, Newcastle upon Tyne, NE4 5PL, UK d Human Nutrition Research Centre, Institute for Ageing and Health, Medical School, University of Newcastle upon Tyne, Framlington Place, Newcastle upon Tyne, NE2 4HH, UK
AuthorAffiliation_xml	– name: b Department of Surgery, Medical School, University of Newcastle upon Tyne, Framlington Place, Newcastle upon Tyne, NE2 4HH, UK – name: d Human Nutrition Research Centre, Institute for Ageing and Health, Medical School, University of Newcastle upon Tyne, Framlington Place, Newcastle upon Tyne, NE2 4HH, UK – name: c Institute for Ageing and Health, Henry Wellcome Laboratory for Biogerontology Research, Newcastle University, Campus for Ageing and Vitality, Newcastle upon Tyne, NE4 5PL, UK – name: a Mitochondrial Research Group, Institute for Ageing and Health, Medical School, University of Newcastle upon Tyne, Framlington Place, Newcastle upon Tyne, NE2 4HH, UK
Author_xml	– sequence: 1 givenname: Laura C. surname: Greaves fullname: Greaves, Laura C. organization: Mitochondrial Research Group, Institute for Ageing and Health, Medical School, University of Newcastle upon Tyne, Framlington Place, Newcastle upon Tyne, NE2 4HH, UK – sequence: 2 givenname: Martin J. surname: Barron fullname: Barron, Martin J. organization: Mitochondrial Research Group, Institute for Ageing and Health, Medical School, University of Newcastle upon Tyne, Framlington Place, Newcastle upon Tyne, NE2 4HH, UK – sequence: 3 givenname: Stefan surname: Plusa fullname: Plusa, Stefan organization: Department of Surgery, Medical School, University of Newcastle upon Tyne, Framlington Place, Newcastle upon Tyne, NE2 4HH, UK – sequence: 4 givenname: Thomas B. surname: Kirkwood fullname: Kirkwood, Thomas B. organization: Institute for Ageing and Health, Henry Wellcome Laboratory for Biogerontology Research, Newcastle University, Campus for Ageing and Vitality, Newcastle upon Tyne, NE4 5PL, UK – sequence: 5 givenname: John C. surname: Mathers fullname: Mathers, John C. organization: Human Nutrition Research Centre, Institute for Ageing and Health, Medical School, University of Newcastle upon Tyne, Framlington Place, Newcastle upon Tyne, NE2 4HH, UK – sequence: 6 givenname: Robert W. surname: Taylor fullname: Taylor, Robert W. organization: Mitochondrial Research Group, Institute for Ageing and Health, Medical School, University of Newcastle upon Tyne, Framlington Place, Newcastle upon Tyne, NE2 4HH, UK – sequence: 7 givenname: Doug M. surname: Turnbull fullname: Turnbull, Doug M. email: d.m.turnbull@ncl.ac.uk organization: Mitochondrial Research Group, Institute for Ageing and Health, Medical School, University of Newcastle upon Tyne, Framlington Place, Newcastle upon Tyne, NE2 4HH, UK
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Snippet	Mitochondrial DNA (mtDNA) mutations accumulate in a number of ageing tissues and are proposed to play a role in the ageing process. We have previously shown...
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SubjectTerms	Adolescent Adult Aged Aged, 80 and over Ageing Aging - genetics Aging - metabolism Aging - pathology Amino Acid Substitution Base Sequence Colon Colon - anatomy & histology Colon - metabolism DNA Mutational Analysis DNA, Mitochondrial - genetics Electron Transport - genetics Electron Transport - physiology Electron Transport Complex I - metabolism Electron Transport Complex II - metabolism Electron Transport Complex III - metabolism Electron Transport Complex IV - metabolism Genome, Mitochondrial Humans Immunohistochemistry Intestinal Mucosa - anatomy & histology Intestinal Mucosa - metabolism Middle Aged Mitochondria Mitochondrial Diseases - genetics Mitochondrial Diseases - metabolism mtDNA Mutation Point Mutation Respiratory chain Young Adult
Title	Defects in multiple complexes of the respiratory chain are present in ageing human colonic crypts
URI	https://dx.doi.org/10.1016/j.exger.2010.01.013 https://www.ncbi.nlm.nih.gov/pubmed/20096767 https://www.proquest.com/docview/733135542 https://pubmed.ncbi.nlm.nih.gov/PMC2887930
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