Bestrijding Black Mold in geoculeerde rozenteelt 2008-2009

Black Mold (Chalaropsis thielavioides) is een schimmel die in 2007 veel schade heeft veroorzaakt in de struikrozen. De schimmel infecteert de oculatiewond met als gevolg dat het oculatieoog niet aanslaat. Op sommige percelen ging tot wel 70% van de enten verloren. In een tweejarig PT project is onderzocht wateen goede beheersingsstrategie voor Black Mold is. Er is gekeken naar de volgende punten: Bestrijding van Black Mold met chemische middelen. In het kader van het ontwikkelen van een bestrijdingsstrategie van Black Mold zijn verschillende middelen getest. Het druppelen van middel T in de T-snede bleek goed te werken tegen Black Mold. Het was echter niet mogelijk Black Mold te bestrijden via de traditionele manier zoals het bespuiten van de stam of de plant in zijn geheel. Ook het bespuiten van de T-snede werkte niet. Het bleek dat Black Mold alleen bestreden kon worden wanneer het bestrijdingsmiddel in de T-snede werd gedruppeld. Resistente onderstammen. In de literatuur waren aanwijzingen gevonden dat er rozenonderstam varianten zouden bestaan die resistent zijn tegen Black Mold. Smid’s Ideal en Multiflora zijn beide in een kas- en veldproef getest en bleken vatbaar voor Black Mold te zijn. Epidemiologie van Black Mold. Verschillende facetten van de epidemiologie van Black Mold zijn onderzocht. het was niet mogelijk een relatie tussen de weersomstandigheden in 2007 en de grootschalige uitbraak van Black Mold vast te stellen. Onder laboratorium condities is uitgezocht dat Black Mold verschillende optimum temperaturen heeft. Zo is de optimum temperatuur voor myceliumgroei 24°C, voor kieming 15°C en voor sporulatie 30°C. Het is echter nog niet duidelijk wat de optimale infectie temperatuur van Black Mold is. Verder is er gekeken of Black Mold in de grond een infectiebron kan zijn. Stukjes peen zijn gebruikt in een lokaastoets omdat Black Mold ook peen infecteert. Met behulp van deze toets kon echter niet worden vastgesteld dat percelen met grootschalige Black Mold uitbraken ook meer stukjes peen aantastten. . Klaarblijkelijk is de hoeveelheid van Black Mold in de grond niet van belang. Verder is gekeken of besmette grond Black Mold infecties kon veroorzaken door de grond op te laten spatten of aan te aarden. Dit bleek niet het geval. Plant materiaal en het oculatiemes zijn waarschijnlijk geen grote infectiebronnen van Black Mold. Het is echter wel gebleken dat Black Mold via het mes verspreid kan worden. Daarom is het effect van mesontsmetting ook onderzocht. Het is aan te raden het mes regelmatig te ontsmetten met spiritus of alcohol

Allelic mutations of the sodium channel SCN8A reveal multiple cellular and physiological functions

Allelic mutations of Scn8a in the mouse have revealed the range of neurological disorders that can result from alternations of one neuronal sodium channel. Null mutations produce the most severe phenotype, with motor neuron failure leading to paralysis and juvenile lethality. Two less severe mutations cause ataxia, tremor, muscle weakness, and dystonia. The electrophysiological effects have been studied at the cellular level by recording from neurons from the mutant mice. The data demonstrate that Scn8a is required for the complex spiking of cerebellar Purkinje cells and for persistent sodium current in several classes of neurons, including some with pacemaker roles. The mouse mutations of Scn8a have also provided insight into the mode of inheritance of channelopathies, and led to the identification of a modifier gene that affects transcript splicing. These mutations demonstrate the value of mouse models to elucidate the pathophysiology of human disease.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/42795/1/10709_2004_Article_5381441.pd

Mutation of FIG4 causes neurodegeneration in the pale tremor mouse and patients with CMT4J

Membrane-bound phosphoinositides are signalling molecules that have a key role in vesicle trafficking in eukaryotic cells(1). Proteins that bind specific phosphoinositides mediate interactions between membrane-bounded compartments whose identity is partially encoded by cytoplasmic phospholipid tags. Little is known about the localization and regulation of mammalian phosphatidylinositol-3,5-bisphosphate ( PtdIns( 3,5)P-2), a phospholipid present in small quantities that regulates membrane trafficking in the endosome - lysosome axis in yeast(2). Here we describe a multi-organ disorder with neuronal degeneration in the central nervous system, peripheral neuronopathy and diluted pigmentation in the 'pale tremor' mouse. Positional cloning identified insertion of ETn2 beta ( early transposon 2 beta)(3) into intron 18 of Fig4 (A530089I17Rik), the homologue of a yeast SAC ( suppressor of actin) domain PtdIns(3,5) P-2 5-phosphatase located in the vacuolar membrane. The abnormal concentration of PtdIns( 3,5) P2 in cultured fibroblasts from pale tremor mice demonstrates the conserved biochemical function of mammalian Fig4. The cytoplasm of fibroblasts from pale tremor mice is filled with large vacuoles that are immunoreactive for LAMP-2 (lysosomal-associated membrane protein 2), consistent with dysfunction of the late endosome - lysosome axis. Neonatal neurodegeneration in sensory and autonomic ganglia is followed by loss of neurons from layers four and five of the cortex, deep cerebellar nuclei and other localized brain regions. The sciatic nerve exhibits reduced numbers of large-diameter myelinated axons, slowed nerve conduction velocity and reduced amplitude of compound muscle action potentials. We identified pathogenic mutations of human FIG4 (KIAA0274) on chromosome 6q21 in four unrelated patients with hereditary motor and sensory neuropathy. This novel form of autosomal recessive Charcot - Marie - Tooth disorder is designated CMT4J.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/62835/1/nature05876.pd

Genomics in neurodevelopmental disorders: an avenue to personalized medicine

Despite the remarkable number of scientific breakthroughs of the last 100 years, the treatment of neurodevelopmental disorders (e.g., autism spectrum disorder, intellectual disability) remains a great challenge. Recent advancements in genomics, such as whole-exome or whole-genome sequencing, have enabled scientists to identify numerous mutations underlying neurodevelopmental disorders. Given the few hundred risk genes that have been discovered, the etiological variability and the heterogeneous clinical presentation, the need for genotype — along with phenotype- based diagnosis of individual patients has become a requisite. In this review we look at recent advancements in genomic analysis and their translation into clinical practice

Observing the cell in its native state: Imaging subcellular dynamics in multicellular organisms

This is the author accepted manuscript. The final version is available from the American Association for the Advancement of Science via the DOI in this recordTrue physiological imaging of subcellular dynamics requires studying cells within their parent organisms, where all the environmental cues that drive gene expression, and hence the phenotypes that we actually observe, are present. A complete understanding also requires volumetric imaging of the cell and its surroundings at high spatiotemporal resolution, without inducing undue stress on either. We combined lattice light-sheet microscopy with adaptive optics to achieve, across large multicellular volumes, noninvasive aberration-free imaging of subcellular processes, including endocytosis, organelle remodeling during mitosis, and the migration of axons, immune cells, and metastatic cancer cells in vivo. The technology reveals the phenotypic diversity within cells across different organisms and developmental stages and may offer insights into how cells harness their intrinsic variability to adapt to different physiological environments.Howard Hughes Medical Institute (HHMI)BiogenIonis PharmaceuticalsNational Institutes of Health (NIH)University of ExeterCarol M. Baldwin FoundationDamon Runyon Cancer Research FoundationNational Science Foundation (NSF)Pew Charitable Trust

Visualizing the metazoan proliferation-quiescence decision in vivo

Cell proliferation and quiescence are intimately coordinated during metazoan development. Here, we adapt a cyclin-dependent kinase (CDK) sensor to uncouple these key events of the cell cycle in Caenorhabditis elegans and zebrafish through live-cell imaging. The CDK sensor consists of a fluorescently tagged CDK substrate that steadily translocates from the nucleus to the cytoplasm in response to increasing CDK activity and consequent sensor phosphorylation. We show that the CDK sensor can distinguish cycling cells in G1 from quiescent cells in G0, revealing a possible commitment point and a cryptic stochasticity in an otherwise invariant C. elegans cell lineage. Finally, we derive a predictive model of future proliferation behavior in C. elegans based on a snapshot of CDK activity in newly born cells. Thus, we introduce a live-cell imaging tool to facilitate in vivo studies of cell-cycle control in a wide-range of developmental contexts. </div

Ocrelizumab versus Interferon Beta-1a in Relapsing Multiple Sclerosis

Supported by F. Hoffmann–La Roche