Dictyostelium, a microbial model for brain disease
Most neurodegenerative diseases are associated with mitochondrial dysfunction. In humans, mutations in mitochondrial genes result in a range of phenotypic outcomes which do not correlate well with the underlying genetic cause. Other neurodegenerative diseases are caused by mutations that affect the...
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| Published in | Biochimica et biophysica acta Vol. 1840; no. 4; pp. 1413 - 1432 |
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| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Netherlands
Elsevier B.V
01.04.2014
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0304-4165 0006-3002 1872-8006 |
| DOI | 10.1016/j.bbagen.2013.10.019 |
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| Abstract | Most neurodegenerative diseases are associated with mitochondrial dysfunction. In humans, mutations in mitochondrial genes result in a range of phenotypic outcomes which do not correlate well with the underlying genetic cause. Other neurodegenerative diseases are caused by mutations that affect the function and trafficking of lysosomes, endosomes and autophagosomes. Many of the complexities of these human diseases can be avoided by studying them in the simple eukaryotic model Dictyostelium discoideum.
This review describes research using Dictyostelium to study cytopathological pathways underlying a variety of neurodegenerative diseases including mitochondrial, lysosomal and vesicle trafficking disorders.
Generalised mitochondrial respiratory deficiencies in Dictyostelium produce a consistent pattern of defective phenotypes that are caused by chronic activation of a cellular energy sensor AMPK (AMP-activated protein kinase) and not ATP deficiency per se. Surprisingly, when individual subunits of Complex I are knocked out, both AMPK-dependent and AMPK-independent, subunit-specific phenotypes are observed. Many nonmitochondrial proteins associated with neurological disorders have homologues in Dictyostelium and are associated with the function and trafficking of lysosomes and endosomes. Conversely, some genes associated with neurodegenerative disorders do not have homologues in Dictyostelium and this provides a unique avenue for studying these mutated proteins in the absence of endogeneous protein.
Using the Dictyostelium model we have gained insights into the sublethal cytopathological pathways whose dysregulation contributes to phenotypic outcomes in neurodegenerative disease. This work is beginning to distinguish correlation, cause and effect in the complex network of cross talk between the various organelles involved. This article is part of a Special Issue entitled Frontiers of Mitochondrial Research
[Display omitted]
•Dictyostelium, an ideal model to study mitochondrial and neurodegenerative disorders•Generalised OXPHOS defects result in common defective phenotypes in Dictyostelium.•Common defective phenotypes are caused by chronic activation of AMPK,•Knockout of complex I subunits results in additional AMPK -independent phenotypes.•Alzheimer's, Parkinson's, Huntington's, lysosomal diseases studied in Dictyostelium, |
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| AbstractList | Most neurodegenerative diseases are associated with mitochondrial dysfunction. In humans, mutations in mitochondrial genes result in a range of phenotypic outcomes which do not correlate well with the underlying genetic cause. Other neurodegenerative diseases are caused by mutations that affect the function and trafficking of lysosomes, endosomes and autophagosomes. Many of the complexities of these human diseases can be avoided by studying them in the simple eukaryotic model Dictyostelium discoideum.BACKGROUNDMost neurodegenerative diseases are associated with mitochondrial dysfunction. In humans, mutations in mitochondrial genes result in a range of phenotypic outcomes which do not correlate well with the underlying genetic cause. Other neurodegenerative diseases are caused by mutations that affect the function and trafficking of lysosomes, endosomes and autophagosomes. Many of the complexities of these human diseases can be avoided by studying them in the simple eukaryotic model Dictyostelium discoideum.This review describes research using Dictyostelium to study cytopathological pathways underlying a variety of neurodegenerative diseases including mitochondrial, lysosomal and vesicle trafficking disorders.SCOPE OF REVIEWThis review describes research using Dictyostelium to study cytopathological pathways underlying a variety of neurodegenerative diseases including mitochondrial, lysosomal and vesicle trafficking disorders.Generalised mitochondrial respiratory deficiencies in Dictyostelium produce a consistent pattern of defective phenotypes that are caused by chronic activation of a cellular energy sensor AMPK (AMP-activated protein kinase) and not ATP deficiency per se. Surprisingly, when individual subunits of Complex I are knocked out, both AMPK-dependent and AMPK-independent, subunit-specific phenotypes are observed. Many nonmitochondrial proteins associated with neurological disorders have homologues in Dictyostelium and are associated with the function and trafficking of lysosomes and endosomes. Conversely, some genes associated with neurodegenerative disorders do not have homologues in Dictyostelium and this provides a unique avenue for studying these mutated proteins in the absence of endogeneous protein.MAJOR CONCLUSIONSGeneralised mitochondrial respiratory deficiencies in Dictyostelium produce a consistent pattern of defective phenotypes that are caused by chronic activation of a cellular energy sensor AMPK (AMP-activated protein kinase) and not ATP deficiency per se. Surprisingly, when individual subunits of Complex I are knocked out, both AMPK-dependent and AMPK-independent, subunit-specific phenotypes are observed. Many nonmitochondrial proteins associated with neurological disorders have homologues in Dictyostelium and are associated with the function and trafficking of lysosomes and endosomes. Conversely, some genes associated with neurodegenerative disorders do not have homologues in Dictyostelium and this provides a unique avenue for studying these mutated proteins in the absence of endogeneous protein.Using the Dictyostelium model we have gained insights into the sublethal cytopathological pathways whose dysregulation contributes to phenotypic outcomes in neurodegenerative disease. This work is beginning to distinguish correlation, cause and effect in the complex network of cross talk between the various organelles involved. This article is part of a Special Issue entitled Frontiers of Mitochondrial Research.GENERAL SIGNIFICANCEUsing the Dictyostelium model we have gained insights into the sublethal cytopathological pathways whose dysregulation contributes to phenotypic outcomes in neurodegenerative disease. This work is beginning to distinguish correlation, cause and effect in the complex network of cross talk between the various organelles involved. This article is part of a Special Issue entitled Frontiers of Mitochondrial Research. Most neurodegenerative diseases are associated with mitochondrial dysfunction. In humans, mutations in mitochondrial genes result in a range of phenotypic outcomes which do not correlate well with the underlying genetic cause. Other neurodegenerative diseases are caused by mutations that affect the function and trafficking of lysosomes, endosomes and autophagosomes. Many of the complexities of these human diseases can be avoided by studying them in the simple eukaryotic model Dictyostelium discoideum.This review describes research using Dictyostelium to study cytopathological pathways underlying a variety of neurodegenerative diseases including mitochondrial, lysosomal and vesicle trafficking disorders.Generalised mitochondrial respiratory deficiencies in Dictyostelium produce a consistent pattern of defective phenotypes that are caused by chronic activation of a cellular energy sensor AMPK (AMP-activated protein kinase) and not ATP deficiency per se. Surprisingly, when individual subunits of Complex I are knocked out, both AMPK-dependent and AMPK-independent, subunit-specific phenotypes are observed. Many nonmitochondrial proteins associated with neurological disorders have homologues in Dictyostelium and are associated with the function and trafficking of lysosomes and endosomes. Conversely, some genes associated with neurodegenerative disorders do not have homologues in Dictyostelium and this provides a unique avenue for studying these mutated proteins in the absence of endogeneous protein.Using the Dictyostelium model we have gained insights into the sublethal cytopathological pathways whose dysregulation contributes to phenotypic outcomes in neurodegenerative disease. This work is beginning to distinguish correlation, cause and effect in the complex network of cross talk between the various organelles involved. This article is part of a Special Issue entitled Frontiers of Mitochondrial Research Most neurodegenerative diseases are associated with mitochondrial dysfunction. In humans, mutations in mitochondrial genes result in a range of phenotypic outcomes which do not correlate well with the underlying genetic cause. Other neurodegenerative diseases are caused by mutations that affect the function and trafficking of lysosomes, endosomes and autophagosomes. Many of the complexities of these human diseases can be avoided by studying them in the simple eukaryotic model Dictyostelium discoideum. This review describes research using Dictyostelium to study cytopathological pathways underlying a variety of neurodegenerative diseases including mitochondrial, lysosomal and vesicle trafficking disorders. Generalised mitochondrial respiratory deficiencies in Dictyostelium produce a consistent pattern of defective phenotypes that are caused by chronic activation of a cellular energy sensor AMPK (AMP-activated protein kinase) and not ATP deficiency per se. Surprisingly, when individual subunits of Complex I are knocked out, both AMPK-dependent and AMPK-independent, subunit-specific phenotypes are observed. Many nonmitochondrial proteins associated with neurological disorders have homologues in Dictyostelium and are associated with the function and trafficking of lysosomes and endosomes. Conversely, some genes associated with neurodegenerative disorders do not have homologues in Dictyostelium and this provides a unique avenue for studying these mutated proteins in the absence of endogeneous protein. Using the Dictyostelium model we have gained insights into the sublethal cytopathological pathways whose dysregulation contributes to phenotypic outcomes in neurodegenerative disease. This work is beginning to distinguish correlation, cause and effect in the complex network of cross talk between the various organelles involved. This article is part of a Special Issue entitled Frontiers of Mitochondrial Research. Most neurodegenerative diseases are associated with mitochondrial dysfunction. In humans, mutations in mitochondrial genes result in a range of phenotypic outcomes which do not correlate well with the underlying genetic cause. Other neurodegenerative diseases are caused by mutations that affect the function and trafficking of lysosomes, endosomes and autophagosomes. Many of the complexities of these human diseases can be avoided by studying them in the simple eukaryotic model Dictyostelium discoideum. This review describes research using Dictyostelium to study cytopathological pathways underlying a variety of neurodegenerative diseases including mitochondrial, lysosomal and vesicle trafficking disorders. Generalised mitochondrial respiratory deficiencies in Dictyostelium produce a consistent pattern of defective phenotypes that are caused by chronic activation of a cellular energy sensor AMPK (AMP-activated protein kinase) and not ATP deficiency per se. Surprisingly, when individual subunits of Complex I are knocked out, both AMPK-dependent and AMPK-independent, subunit-specific phenotypes are observed. Many nonmitochondrial proteins associated with neurological disorders have homologues in Dictyostelium and are associated with the function and trafficking of lysosomes and endosomes. Conversely, some genes associated with neurodegenerative disorders do not have homologues in Dictyostelium and this provides a unique avenue for studying these mutated proteins in the absence of endogeneous protein. Using the Dictyostelium model we have gained insights into the sublethal cytopathological pathways whose dysregulation contributes to phenotypic outcomes in neurodegenerative disease. This work is beginning to distinguish correlation, cause and effect in the complex network of cross talk between the various organelles involved. This article is part of a Special Issue entitled Frontiers of Mitochondrial Research [Display omitted] •Dictyostelium, an ideal model to study mitochondrial and neurodegenerative disorders•Generalised OXPHOS defects result in common defective phenotypes in Dictyostelium.•Common defective phenotypes are caused by chronic activation of AMPK,•Knockout of complex I subunits results in additional AMPK -independent phenotypes.•Alzheimer's, Parkinson's, Huntington's, lysosomal diseases studied in Dictyostelium, |
| Author | Sanislav, O. De Piazza, S.W. Chen, S. Francione, L.M. Storey, C.L. Smith, P.K. Fernando, S.G. Annesley, S.J. Ilievska, J. Fisher, P.R. Chavan, A.J. Lay, S.T. Farah, C. |
| Author_xml | – sequence: 1 givenname: S.J. surname: Annesley fullname: Annesley, S.J. – sequence: 2 givenname: S. surname: Chen fullname: Chen, S. – sequence: 3 givenname: L.M. surname: Francione fullname: Francione, L.M. – sequence: 4 givenname: O. surname: Sanislav fullname: Sanislav, O. – sequence: 5 givenname: A.J. surname: Chavan fullname: Chavan, A.J. – sequence: 6 givenname: C. surname: Farah fullname: Farah, C. – sequence: 7 givenname: S.W. surname: De Piazza fullname: De Piazza, S.W. – sequence: 8 givenname: C.L. surname: Storey fullname: Storey, C.L. – sequence: 9 givenname: J. surname: Ilievska fullname: Ilievska, J. – sequence: 10 givenname: S.G. surname: Fernando fullname: Fernando, S.G. – sequence: 11 givenname: P.K. surname: Smith fullname: Smith, P.K. – sequence: 12 givenname: S.T. surname: Lay fullname: Lay, S.T. – sequence: 13 givenname: P.R. surname: Fisher fullname: Fisher, P.R. email: P.Fisher@latrobe.edu.au |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24161926$$D View this record in MEDLINE/PubMed |
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| Keywords | AMPK OXPHOS Lysosomal disease Dictyostelium neurodegenerative disease Mitochondrial disease |
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| PublicationDate | 2014-04-01 |
| PublicationDateYYYYMMDD | 2014-04-01 |
| PublicationDate_xml | – month: 04 year: 2014 text: 2014-04-01 day: 01 |
| PublicationDecade | 2010 |
| PublicationPlace | Netherlands |
| PublicationPlace_xml | – name: Netherlands |
| PublicationTitle | Biochimica et biophysica acta |
| PublicationTitleAlternate | Biochim Biophys Acta |
| PublicationYear | 2014 |
| Publisher | Elsevier B.V |
| Publisher_xml | – name: Elsevier B.V |
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| SubjectTerms | adenosine triphosphate AMP-activated protein kinase AMP-Activated Protein Kinases - genetics AMP-Activated Protein Kinases - metabolism AMPK biological models brain Brain Diseases, Metabolic - metabolism Brain Diseases, Metabolic - pathology Dictyostelium Dictyostelium - genetics Dictyostelium - metabolism Dictyostelium - ultrastructure endosomes energy genes human diseases Humans Lysosomal disease lysosomes mitochondria Mitochondria - genetics Mitochondria - metabolism Mitochondrial disease Mitochondrial Diseases - metabolism Mitochondrial Diseases - pathology Models, Neurological mutation neurodegenerative disease neurodegenerative diseases Organisms, Genetically Modified Oxidative Phosphorylation OXPHOS phenotype physiological transport proteins |
| Title | Dictyostelium, a microbial model for brain disease |
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