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  • 1
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    Neuroscience. The meaning of a mini (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-07-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Verstreken, P -- Bellen, H J -- New York, N.Y. -- Science. 2001 Jul 20;293(5529):443-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Human Genetics, Division of Neuroscience, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11463902" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Drosophila/genetics/physiology ; Membrane Potentials/physiology ; Mice ; Mutation ; Neuromuscular Junction/*physiology ; Receptor Aggregation ; Receptors, Cholinergic/physiology ; Receptors, Glutamate/*metabolism ; Synaptic Membranes/*physiology ; *Synaptic Transmission ; Synaptic Vesicles/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Conditional mutagenesis in Drosophila (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-04-04
    Description: Most genes function at multiple stages of metazoan development, in dividing and nondividing cells. Generating mouse conditional knock-outs (cKO), where a gene can be eliminated in a temporally and spatially controlled manner, is a valuable technique because it allows study of gene function at any stage of life. In contrast and despite the development of many other powerful genetic tools, cKO has thus far been lacking in Drosophila. We combined several recent molecular and genetic technical advances in an approach termed integrase-mediated approach for gene knock-out (IMAGO). IMAGO allows the replacement of any genomic sequence, such as a gene, with another desired sequence, including cKO alleles that can be used to create positively marked mutant cells. IMAGO should also be applicable to other genetic model organisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Choi, Ching Man -- Vilain, Sven -- Langen, Marion -- Van Kelst, Sofie -- De Geest, Natalie -- Yan, Jiekun -- Verstreken, Patrik -- Hassan, Bassem A -- New York, N.Y. -- Science. 2009 Apr 3;324(5923):54. doi: 10.1126/science.1168275.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Developmental Genetics, VIB 3000 Leuven, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19342580" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Drosophila melanogaster/cytology/*genetics ; *Gene Knockout Techniques ; Genes, Insect ; Integrases/metabolism ; Molecular Sequence Data ; *Mutagenesis ; Nerve Tissue Proteins/genetics ; Photoreceptor Cells, Invertebrate/cytology/physiology ; Recombination, Genetic ; Sense Organs/cytology/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Vitamin K2 is a mitochondrial electron carrier that rescues pink1 deficiency (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-15
    Description: Human UBIAD1 localizes to mitochondria and converts vitamin K(1) to vitamin K(2). Vitamin K(2) is best known as a cofactor in blood coagulation, but in bacteria it is a membrane-bound electron carrier. Whether vitamin K(2) exerts a similar carrier function in eukaryotic cells is unknown. We identified Drosophila UBIAD1/Heix as a modifier of pink1, a gene mutated in Parkinson's disease that affects mitochondrial function. We found that vitamin K(2) was necessary and sufficient to transfer electrons in Drosophila mitochondria. Heix mutants showed severe mitochondrial defects that were rescued by vitamin K(2), and, similar to ubiquinone, vitamin K(2) transferred electrons in Drosophila mitochondria, resulting in more efficient adenosine triphosphate (ATP) production. Thus, mitochondrial dysfunction was rescued by vitamin K(2) that serves as a mitochondrial electron carrier, helping to maintain normal ATP production.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vos, Melissa -- Esposito, Giovanni -- Edirisinghe, Janaka N -- Vilain, Sven -- Haddad, Dominik M -- Slabbaert, Jan R -- Van Meensel, Stefanie -- Schaap, Onno -- De Strooper, Bart -- Meganathan, R -- Morais, Vanessa A -- Verstreken, Patrik -- New York, N.Y. -- Science. 2012 Jun 8;336(6086):1306-10. doi: 10.1126/science.1218632. Epub 2012 May 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉VIB Center for the Biology of Disease, Leuven, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22582012" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Drosophila/genetics/*metabolism ; Drosophila Proteins/deficiency/*genetics/*metabolism ; *Electron Transport ; Escherichia coli/metabolism ; Flight, Animal ; Genes, Insect ; Membrane Potential, Mitochondrial ; Mitochondria/*metabolism/ultrastructure ; Mitochondria, Muscle/metabolism/ultrastructure ; Mutation ; Oxygen Consumption ; Protein-Serine-Threonine Kinases/deficiency/*genetics/*metabolism ; Ubiquinone/metabolism ; Ubiquitin-Protein Ligases/genetics ; Vitamin K 2/*metabolism/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    PINK1 loss-of-function mutations affect mitochondrial complex I activity via NdufA10 ubiquinone uncoupling (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-03-22
    Description: Under resting conditions, Pink1 knockout cells and cells derived from patients with PINK1 mutations display a loss of mitochondrial complex I reductive activity, causing a decrease in the mitochondrial membrane potential. Analyzing the phosphoproteome of complex I in liver and brain from Pink1(-/-) mice, we found specific loss of phosphorylation of serine-250 in complex I subunit NdufA10. Phosphorylation of serine-250 was needed for ubiquinone reduction by complex I. Phosphomimetic NdufA10 reversed Pink1 deficits in mouse knockout cells and rescued mitochondrial depolarization and synaptic transmission defects in pink(B9)-null mutant Drosophila. Complex I deficits and adenosine triphosphate synthesis were also rescued in cells derived from PINK1 patients. Thus, this evolutionary conserved pathway may contribute to the pathogenic cascade that eventually leads to Parkinson's disease in patients with PINK1 mutations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morais, Vanessa A -- Haddad, Dominik -- Craessaerts, Katleen -- De Bock, Pieter-Jan -- Swerts, Jef -- Vilain, Sven -- Aerts, Liesbeth -- Overbergh, Lut -- Grunewald, Anne -- Seibler, Philip -- Klein, Christine -- Gevaert, Kris -- Verstreken, Patrik -- De Strooper, Bart -- New York, N.Y. -- Science. 2014 Apr 11;344(6180):203-7. doi: 10.1126/science.1249161. Epub 2014 Mar 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉VIB Center for the Biology of Disease, 3000 Leuven, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24652937" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Brain/enzymology ; Drosophila Proteins/*metabolism ; Electron Transport Complex I/*metabolism ; Humans ; Liver/enzymology ; Membrane Potential, Mitochondrial/genetics ; Mice ; Mice, Knockout ; Molecular Sequence Data ; Mutation ; NADH Dehydrogenase/*metabolism ; Parkinson Disease/*enzymology/*genetics ; Phosphorylation/genetics ; Protein Kinases/*genetics ; Proteome ; Serine/chemistry/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 5
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    Mapping Drosophila mutations with molecularly defined P element insertions (2003)
    National Academy of Sciences
    Details
    Publication Date: 2003-09-05
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 6
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    WASP is activated by phosphatidylinositol-4,5-bisphosphate to restrict synapse growth in a pathway parallel to bone morphogenetic protein signaling (2010)
    National Academy of Sciences
    Details
    Publication Date: 2010-09-15
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 7
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    Alternative oxidase rescues mitochondria-mediated dopaminergic cell loss in Drosophila (2012)
    Oxford University Press
    Details
    Publication Date: 2012-05-25
    Description: Mitochondrial dysfunction is commonly observed in degenerative disorders, including Alzheimer's and Parkinson's disease that are characterized by the progressive and selective loss of neuronal subpopulations. It is currently unclear, however, whether mitochondrial dysfunction is primary or secondary to other pathogenic processes that eventually lead to age-related neurodegeneration. Here we establish an in vivo Drosophila model of mitochondrial dysfunction by downregulating the catalytic subunit of mitochondrial DNA (mtDNA) polymerase in cholinergic, serotonergic and dopaminergic neurons. The resulting flies are characterized by lowered respiratory chain activity, premature aging, age-related motor deficits as well as adult onset, progressive and cell-type-specific, dopaminergic neurodegeneration. Using this model, we find that associated lethality can be partially rescued by targeting PINK1/parkin signaling or Drp1, both of which have been implicated in mitochondrial dynamics and Parkinson's disease. Bypassing mitochondrial complex III/IV deficiencies with Alternative oxidase ( AOX ), however, fully restores ATP levels and prevents dopaminergic neurodegeneration. In contrast, ATP levels and neurodegeneration are not rescued when mitochondrial complex I deficiencies are bypassed with NADH-Q oxidoreductase . Our results demonstrate that mtDNA-mediated mitochondrial dysfunction can cause age-related and cell-type-specific neurodegeneration which AOX is able to alleviate and indicate that AOX or its surrogates may prove useful as a therapeutic tool for limiting respiratory chain deficiencies caused by mtDNA decline in healthy aging and neurodegenerative disease.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 8
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    The deubiquitinase USP15 antagonizes Parkin-mediated mitochondrial ubiquitination and mitophagy (2014)
    Oxford University Press
    Details
    Publication Date: 2014-09-10
    Description: Loss-of-function mutations in PARK2 , the gene encoding the E3 ubiquitin ligase Parkin, are the most frequent cause of recessive Parkinson's disease (PD). Parkin translocates from the cytosol to depolarized mitochondria, ubiquitinates outer mitochondrial membrane proteins and induces selective autophagy of the damaged mitochondria (mitophagy). Here, we show that ubiquitin-specific protease 15 (USP15), a deubiquitinating enzyme (DUB) widely expressed in brain and other organs, opposes Parkin-mediated mitophagy, while a panel of other DUBs and a catalytically inactive version of USP15 do not. Moreover, knockdown of USP15 rescues the mitophagy defect of PD patient fibroblasts with PARK2 mutations and decreased Parkin levels. USP15 does not affect the ubiquitination status of Parkin or Parkin translocation to mitochondria, but counteracts Parkin-mediated mitochondrial ubiquitination. Knockdown of the DUB CG8334, the closest homolog of USP15 in Drosophila , largely rescues the mitochondrial and behavioral defects of parkin RNAi flies. These data identify USP15 as an antagonist of Parkin and suggest that USP15 inhibition could be a therapeutic strategy for PD cases caused by reduced Parkin levels.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 9
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    Fast and Efficient Drosophila melanogaster Gene Knock-Ins Using MiMIC Transposons (2014)
    Genetics Society of America (GSA)
    Details
    Publication Date: 2014-12-16
    Description: Modern molecular genetics studies necessitate the manipulation of genes in their endogenous locus, but most of the current methodologies require an inefficient donor-dependent homologous recombination step to locally modify the genome. Here we describe a methodology to efficiently generate Drosophila knock-in alleles by capitalizing on the availability of numerous genomic MiMIC transposon insertions carrying recombinogenic attP sites. Our methodology entails the efficient PhiC31-mediated integration of a recombination cassette flanked by unique I-SceI and/or I-CreI restriction enzyme sites into an attP -site. These restriction enzyme sites allow for double-strand break–mediated removal of unwanted flanking transposon sequences, while leaving the desired genomic modifications or recombination cassettes. As a proof-of-principle, we mutated LRRK , tau , and sky by using different MiMIC elements. We replaced 6 kb of genomic DNA encompassing the tau locus and 35 kb encompassing the sky locus with a recombination cassette that permits easy integration of DNA at these loci and we also generated a functional LRRK HA knock in allele. Given that ~92% of the Drosophila genes are located within the vicinity (〈35 kb) of a MiMIC element, our methodology enables the efficient manipulation of nearly every locus in the fruit fly genome without the need for inefficient donor-dependent homologous recombination events.
    Electronic ISSN: 2160-1836
    Topics: Biology
    Published by Genetics Society of America (GSA)
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  • 10
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    Parkinson's disease: convergence on synaptic homeostasis (2018)
    Springer Nature
    Details
    Publication Date: 2018
    Description: 〈p〉Parkinson's disease, the second most common neurodegenerative disorder, affects millions of people globally. There is no cure, and its prevalence will double by 2030. In recent years, numerous causative genes and risk factors for Parkinson's disease have been identified and more than half appear to function at the synapse. Subtle synaptic defects are thought to precede blunt neuronal death, but the mechanisms that are dysfunctional at synapses are only now being unraveled. Here, we review recent work and propose a model where different Parkinson proteins interact in a cell compartment-specific manner at the synapse where these proteins regulate endocytosis and autophagy. While this field is only recently emerging, the work suggests that the loss of synaptic homeostasis may contribute to neurodegeneration and is a key player in Parkinson's disease.〈/p〉
    Print ISSN: 0261-4189
    Electronic ISSN: 1460-2075
    Topics: Biology , Medicine
    Published by Springer Nature on behalf of The European Molecular Biology Organization (EMBO).
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