Zhao Q, Chen GD, Feng XL, Yu Y, He RR, Li XX, Huang Y, Zhou WX, Guo LD, Zheng YZ, Yao XS, Gao H. Nodulisporiviridins A-H, Bioactive Viridins from Nodulisporium sp. J Nat Prod. 2015 Jun 26;78(6):1221-30. PMID: 25978520.
From the abstract: "Eight new viridins, nodulisporiviridins A-H (1-8), were isolated from the extract of an endolichenic fungal strain Nodulisporium sp. (No. 65-17-2-1) that was fermented with potato-dextrose broth. ... The short-term memory assay on an Aβ transgenic drosophila model of Alzheimer's disease showed that all eight compounds improved the short-term memory capacity, with potencies close to that of the positive control (memantine)."
Wednesday, October 26, 2016
Fly eye study related to Alzheimer's disease
Cutler T, Sarkar A, Moran M, Steffensmeier A, Puli OR, Mancini G, Tare M, Gogia N, Singh A. Drosophila Eye Model to Study Neuroprotective Role of CREB Binding Protein (CBP) in Alzheimer's Disease. PLoS One. 2015 Sep 14;10(9):e0137691. PMID: 26367392; PMCID: PMC4569556.
Characterization of sleep in a fly model of epilepsy
Petruccelli E, Lansdon P, Kitamoto T. Exaggerated Nighttime Sleep and Defective Sleep Homeostasis in a Drosophila Knock-In Model of Human Epilepsy. PLoS One. 2015 Sep 11;10(9):e0137758. PMID: 26361221; PMCID: PMC4567262.
From the abstract: "Despite an established link between epilepsy and sleep behavior, it remains unclear how specific epileptogenic mutations affect sleep and subsequently influence seizure susceptibility. ... Here, we show that at room temperature the GEFS+ mutation dominantly modifies sleep, with mutants exhibiting rapid sleep onset at dusk and increased nighttime sleep as compared to controls. ... Additionally, analyses under other light conditions suggested that the GEFS+ mutation led to reduced buffering of behavioral responses to light on and off stimuli, which contributed to characteristic GEFS+ sleep phenotypes. ... Our study has revealed the sleep architecture of a Drosophila VGSC mutant that harbors a human GEFS+ mutation, and provided unique insight into the relationship between sleep and epilepsy."
From the abstract: "Despite an established link between epilepsy and sleep behavior, it remains unclear how specific epileptogenic mutations affect sleep and subsequently influence seizure susceptibility. ... Here, we show that at room temperature the GEFS+ mutation dominantly modifies sleep, with mutants exhibiting rapid sleep onset at dusk and increased nighttime sleep as compared to controls. ... Additionally, analyses under other light conditions suggested that the GEFS+ mutation led to reduced buffering of behavioral responses to light on and off stimuli, which contributed to characteristic GEFS+ sleep phenotypes. ... Our study has revealed the sleep architecture of a Drosophila VGSC mutant that harbors a human GEFS+ mutation, and provided unique insight into the relationship between sleep and epilepsy."
Green-glowing flies used in study relevant to Huntington's disease
Babcock DT, Ganetzky B. Transcellular spreading of huntingtin aggregates in the Drosophila brain. Proc Natl Acad Sci U S A. 2015 Sep 29;112(39):E5427-33. PMID: 26351672; PMCID: PMC4593132.
From the abstract: "A key feature of many neurodegenerative diseases is the accumulation and subsequent aggregation of misfolded proteins. Recent studies have highlighted the transcellular propagation of protein aggregates in several major neurodegenerative diseases, although the precise mechanisms underlying this spreading and how it relates to disease pathology remain unclear. Here we use a polyglutamine-expanded form of human huntingtin (Htt) with a fluorescent tag to monitor the spreading of aggregates in the Drosophila brain in a model of Huntington's disease. ... We show that Htt aggregates cause non-cell-autonomous pathology ..."
From the abstract: "A key feature of many neurodegenerative diseases is the accumulation and subsequent aggregation of misfolded proteins. Recent studies have highlighted the transcellular propagation of protein aggregates in several major neurodegenerative diseases, although the precise mechanisms underlying this spreading and how it relates to disease pathology remain unclear. Here we use a polyglutamine-expanded form of human huntingtin (Htt) with a fluorescent tag to monitor the spreading of aggregates in the Drosophila brain in a model of Huntington's disease. ... We show that Htt aggregates cause non-cell-autonomous pathology ..."
Uncovering cellular mechanisms relevant to Parkinson's Disease
Dodson MW, Leung LK, Lone M, Lizzio MA, Guo M. Novel ethyl methanesulfonate (EMS)-induced null alleles of the Drosophila homolog of LRRK2 reveal a crucial role in endolysosomal functions and autophagy in vivo. Dis Model Mech. 2014 Dec;7(12):1351-63. PMID: 25288684; PMCID: PMC4257004.
Zhou ZD, Xie SP, Sathiyamoorthy S, Saw WT, Sing TY, Ng SH, Chua HP, Tang AM, Shaffra F, Li Z, Wang H, Ho PG, Lai MK, Angeles DC, Lim TM, Tan EK. F-box protein 7 mutations promote protein aggregation in mitochondria and inhibit mitophagy. Hum Mol Genet. 2015 Nov 15;24(22):6314-30. PMID: 26310625.
Kong Y, Liang X, Liu L, Zhang D, Wan C, Gan Z, Yuan L. High Throughput Sequencing Identifies MicroRNAs Mediating α-Synuclein Toxicity by Targeting Neuroactive-Ligand Receptor Interaction Pathway in Early Stage of Drosophila Parkinson's Disease Model. PLoS One. 2015 Sep 11;10(9):e0137432. PMID: 26361355; PMCID: PMC4567341.
Gehrke S, Wu Z, Klinkenberg M, Sun Y, Auburger G, Guo S, Lu B. PINK1 and Parkin control localized translation of respiratory chain component mRNAs on mitochondria outer membrane. Cell Metab. 2015 Jan 6;21(1):95-108. PMID: 25565208; PMCID: PMC4455944.
Shmueli MD, Schnaider L, Herzog G, Gazit E, Segal D. Computational and experimental characterization of dVHL establish a Drosophila model of VHL syndrome. PLoS One. 2014 Oct 13;9(10):e109864. PMID: 25310726; PMCID: PMC4195687.
Dubos A, Castells-Nobau A, Meziane H, Oortveld MA, Houbaert X, Iacono G, Martin C, Mittelhaeuser C, Lalanne V, Kramer JM, Bhukel A, Quentin C, Slabbert J, Verstreken P, Sigrist SJ, Messaddeq N, Birling MC, Selloum M, Stunnenberg HG, Humeau Y, Schenck A, Herault Y. Conditional depletion of intellectual disability and Parkinsonism candidate gene ATP6AP2 in fly and mouse induces cognitive impairment and neurodegeneration. Hum Mol Genet. 2015 Dec 1;24(23):6736-55. PMID: 26376863; PMCID: PMC4634377.
Arsenijevic Y. Cell Cycle Proteins and Retinal Degeneration: Evidences of New Potential Therapeutic Targets. Adv Exp Med Biol. 2016;854:371-7. PMID: 26427434.
Angelova PR, Agrawalla BK, Elustondo PA, Gordon J, Shiba T, Abramov AY, Chang YT, Pavlov EV. In situ investigation of mammalian inorganic polyphosphate localization using novel selective fluorescent probes JC-D7 and JC-D8. ACS Chem Biol. 2014 Sep 19;9(9):2101-10. PMID: 25007079.
van der Merwe C, Jalali Sefid Dashti Z, Christoffels A, Loos B, Bardien S. Evidence for a common biological pathway linking three Parkinson's disease-causing genes: parkin, PINK1 and DJ-1. Eur J Neurosci. 2015 May;41(9):1113-25. PMID: 25761903.
Zhou ZD, Xie SP, Sathiyamoorthy S, Saw WT, Sing TY, Ng SH, Chua HP, Tang AM, Shaffra F, Li Z, Wang H, Ho PG, Lai MK, Angeles DC, Lim TM, Tan EK. F-box protein 7 mutations promote protein aggregation in mitochondria and inhibit mitophagy. Hum Mol Genet. 2015 Nov 15;24(22):6314-30. PMID: 26310625.
Kong Y, Liang X, Liu L, Zhang D, Wan C, Gan Z, Yuan L. High Throughput Sequencing Identifies MicroRNAs Mediating α-Synuclein Toxicity by Targeting Neuroactive-Ligand Receptor Interaction Pathway in Early Stage of Drosophila Parkinson's Disease Model. PLoS One. 2015 Sep 11;10(9):e0137432. PMID: 26361355; PMCID: PMC4567341.
Gehrke S, Wu Z, Klinkenberg M, Sun Y, Auburger G, Guo S, Lu B. PINK1 and Parkin control localized translation of respiratory chain component mRNAs on mitochondria outer membrane. Cell Metab. 2015 Jan 6;21(1):95-108. PMID: 25565208; PMCID: PMC4455944.
Shmueli MD, Schnaider L, Herzog G, Gazit E, Segal D. Computational and experimental characterization of dVHL establish a Drosophila model of VHL syndrome. PLoS One. 2014 Oct 13;9(10):e109864. PMID: 25310726; PMCID: PMC4195687.
Dubos A, Castells-Nobau A, Meziane H, Oortveld MA, Houbaert X, Iacono G, Martin C, Mittelhaeuser C, Lalanne V, Kramer JM, Bhukel A, Quentin C, Slabbert J, Verstreken P, Sigrist SJ, Messaddeq N, Birling MC, Selloum M, Stunnenberg HG, Humeau Y, Schenck A, Herault Y. Conditional depletion of intellectual disability and Parkinsonism candidate gene ATP6AP2 in fly and mouse induces cognitive impairment and neurodegeneration. Hum Mol Genet. 2015 Dec 1;24(23):6736-55. PMID: 26376863; PMCID: PMC4634377.
Arsenijevic Y. Cell Cycle Proteins and Retinal Degeneration: Evidences of New Potential Therapeutic Targets. Adv Exp Med Biol. 2016;854:371-7. PMID: 26427434.
Angelova PR, Agrawalla BK, Elustondo PA, Gordon J, Shiba T, Abramov AY, Chang YT, Pavlov EV. In situ investigation of mammalian inorganic polyphosphate localization using novel selective fluorescent probes JC-D7 and JC-D8. ACS Chem Biol. 2014 Sep 19;9(9):2101-10. PMID: 25007079.
van der Merwe C, Jalali Sefid Dashti Z, Christoffels A, Loos B, Bardien S. Evidence for a common biological pathway linking three Parkinson's disease-causing genes: parkin, PINK1 and DJ-1. Eur J Neurosci. 2015 May;41(9):1113-25. PMID: 25761903.
Characterization of a fly model of glassic galactosemia
Jumbo-Lucioni P, Parkinson W, Broadie K. Overelaborated synaptic architecture and reduced synaptomatrix glycosylation in a Drosophila classic galactosemia disease model. Dis Model Mech. 2014 Dec;7(12):1365-78. PMID: 25326312; PMCID: PMC4257005.
From the abstract: "Classic galactosemia (CG) is an autosomal recessive disorder resulting from loss of galactose-1-phosphate uridyltransferase (GALT), which catalyzes conversion of galactose-1-phosphate and uridine diphosphate (UDP)-glucose to glucose-1-phosphate and UDP-galactose, immediately upstream of UDP-N-acetylgalactosamine and UDP-N-acetylglucosamine synthesis. These four UDP-sugars are essential donors for driving the synthesis of glycoproteins and glycolipids, which heavily decorate cell surfaces and extracellular spaces. In addition to acute, potentially lethal neonatal symptoms, maturing individuals with CG develop striking neurodevelopmental, motor and cognitive impairments. Previous studies suggest that neurological symptoms are associated with glycosylation defects, with CG recently being described as a congenital disorder of glycosylation (CDG), showing defects in both N- and O-linked glycans. Here, we characterize behavioral traits, synaptic development and glycosylated synaptomatrix formation in a GALT-deficient Drosophila disease model. ... These results reveal synaptomatrix glycosylation losses, altered trans-synaptic signaling pathway components, defective synaptogenesis and impaired coordinated movement in a CG neurological disease model."
From the abstract: "Classic galactosemia (CG) is an autosomal recessive disorder resulting from loss of galactose-1-phosphate uridyltransferase (GALT), which catalyzes conversion of galactose-1-phosphate and uridine diphosphate (UDP)-glucose to glucose-1-phosphate and UDP-galactose, immediately upstream of UDP-N-acetylgalactosamine and UDP-N-acetylglucosamine synthesis. These four UDP-sugars are essential donors for driving the synthesis of glycoproteins and glycolipids, which heavily decorate cell surfaces and extracellular spaces. In addition to acute, potentially lethal neonatal symptoms, maturing individuals with CG develop striking neurodevelopmental, motor and cognitive impairments. Previous studies suggest that neurological symptoms are associated with glycosylation defects, with CG recently being described as a congenital disorder of glycosylation (CDG), showing defects in both N- and O-linked glycans. Here, we characterize behavioral traits, synaptic development and glycosylated synaptomatrix formation in a GALT-deficient Drosophila disease model. ... These results reveal synaptomatrix glycosylation losses, altered trans-synaptic signaling pathway components, defective synaptogenesis and impaired coordinated movement in a CG neurological disease model."
Fly study uncovers new information regarding the cellular role of the ALS related gene TDP-43
Miskiewicz K, Jose LE, Yeshaw WM, Valadas JS, Swerts J, Munck S, Feiguin F, Dermaut B, Verstreken P. HDAC6 is a Bruchpilot deacetylase that facilitates neurotransmitter release. Cell Rep. 2014 Jul 10;8(1):94-102. PMID: 24981865.
From the abstract: "... reduced levels of HDAC6 or increased levels of ELP3, a Bruchpilot acetyltransferase, rescue the presynaptic density defects in TDP-43-expressing flies as well as the decreased adult locomotion ..."
From the abstract: "... reduced levels of HDAC6 or increased levels of ELP3, a Bruchpilot acetyltransferase, rescue the presynaptic density defects in TDP-43-expressing flies as well as the decreased adult locomotion ..."
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