دورية أكاديمية
Diverse cytopathologies in mitochondrial disease are caused by AMP-activated protein kinase signaling.
العنوان: | Diverse cytopathologies in mitochondrial disease are caused by AMP-activated protein kinase signaling. |
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المؤلفون: | Bokko PB; Department of Microbiology, La Trobe University, Melbourne, Victoria 3086, Australia., Francione L, Bandala-Sanchez E, Ahmed AU, Annesley SJ, Huang X, Khurana T, Kimmel AR, Fisher PR |
المصدر: | Molecular biology of the cell [Mol Biol Cell] 2007 May; Vol. 18 (5), pp. 1874-86. Date of Electronic Publication: 2007 Mar 01. |
نوع المنشور: | Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't |
اللغة: | English |
بيانات الدورية: | Publisher: American Society for Cell Biology Country of Publication: United States NLM ID: 9201390 Publication Model: Print-Electronic Cited Medium: Print ISSN: 1059-1524 (Print) Linking ISSN: 10591524 NLM ISO Abbreviation: Mol Biol Cell Subsets: MEDLINE |
أسماء مطبوعة: | Original Publication: Bethesda, MD : American Society for Cell Biology, c1992- |
مواضيع طبية MeSH: | Mitochondrial Diseases/*enzymology , Mitochondrial Diseases/*pathology , Multienzyme Complexes/*metabolism , Protein Serine-Threonine Kinases/*metabolism, AMP-Activated Protein Kinases ; Adenosine Triphosphate/biosynthesis ; Amino Acid Sequence ; Animals ; Base Sequence ; DNA, Protozoan/genetics ; Dictyostelium/enzymology ; Dictyostelium/genetics ; Dictyostelium/growth & development ; Gene Dosage ; Genes, Protozoan ; Humans ; Mitochondrial Diseases/genetics ; Models, Biological ; Molecular Sequence Data ; Multienzyme Complexes/antagonists & inhibitors ; Multienzyme Complexes/chemistry ; Multienzyme Complexes/genetics ; Phagocytosis ; Photobiology ; Pinocytosis ; Protein Serine-Threonine Kinases/antagonists & inhibitors ; Protein Serine-Threonine Kinases/chemistry ; Protein Serine-Threonine Kinases/genetics ; Protein Structure, Tertiary ; Recombinant Proteins/chemistry ; Recombinant Proteins/genetics ; Recombinant Proteins/metabolism ; Signal Transduction |
مستخلص: | The complex cytopathology of mitochondrial diseases is usually attributed to insufficient ATP. AMP-activated protein kinase (AMPK) is a highly sensitive cellular energy sensor that is stimulated by ATP-depleting stresses. By antisense-inhibiting chaperonin 60 expression, we produced mitochondrially diseased strains with gene dose-dependent defects in phototaxis, growth, and multicellular morphogenesis. Mitochondrial disease was phenocopied in a gene dose-dependent manner by overexpressing a constitutively active AMPK alpha subunit (AMPKalphaT). The aberrant phenotypes in mitochondrially diseased strains were suppressed completely by antisense-inhibiting AMPKalpha expression. Phagocytosis and macropinocytosis, although energy consuming, were unaffected by mitochondrial disease and AMPKalpha expression levels. Consistent with the role of AMPK in energy homeostasis, mitochondrial "mass" and ATP levels were reduced by AMPKalpha antisense inhibition and increased by AMPKalphaT overexpression, but they were near normal in mitochondrially diseased cells. We also found that 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside, a pharmacological AMPK activator in mammalian cells, mimics mitochondrial disease in impairing Dictyostelium phototaxis and that AMPKalpha antisense-inhibited cells were resistant to this effect. The results show that diverse cytopathologies in Dictyostelium mitochondrial disease are caused by chronic AMPK signaling not by insufficient ATP. |
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معلومات مُعتمدة: | United States Intramural NIH HHS |
المشرفين على المادة: | 0 (DNA, Protozoan) 0 (Multienzyme Complexes) 0 (Recombinant Proteins) 8L70Q75FXE (Adenosine Triphosphate) EC 2.7.11.1 (Protein Serine-Threonine Kinases) EC 2.7.11.31 (AMP-Activated Protein Kinases) |
تواريخ الأحداث: | Date Created: 20070303 Date Completed: 20070711 Latest Revision: 20211203 |
رمز التحديث: | 20240628 |
مُعرف محوري في PubMed: | PMC1855013 |
DOI: | 10.1091/mbc.e06-09-0881 |
PMID: | 17332500 |
قاعدة البيانات: | MEDLINE |
تدمد: | 1059-1524 |
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DOI: | 10.1091/mbc.e06-09-0881 |