Investigation on the partial resistance of Cpkk2 knock out strain of Cryphonectria parasitica to infection from Cryphonectria hypovirus 1. (Abstract/Comunicazione in atti di convegno)

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  • Investigation on the partial resistance of Cpkk2 knock out strain of Cryphonectria parasitica to infection from Cryphonectria hypovirus 1. (Abstract/Comunicazione in atti di convegno) (literal)
Anno
  • 2014-01-01T00:00:00+01:00 (literal)
Alternative label
  • Turina M., Rossi M. (2014)
    Investigation on the partial resistance of Cpkk2 knock out strain of Cryphonectria parasitica to infection from Cryphonectria hypovirus 1.
    in The Third International Mycovirus Symposium, August 2-5, 2014 Burlington, VT 05405, Burlington, VT USA, August 2-5, 2014
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Turina M., Rossi M. (literal)
Note
  • Comunicazione (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • . (literal)
Titolo
  • Investigation on the partial resistance of Cpkk2 knock out strain of Cryphonectria parasitica to infection from Cryphonectria hypovirus 1. (literal)
Abstract
  • Interaction and interference of Cryphonectria hypovirus 1 (CHV1) infection on various elements of the host signal transduction pathways have been the subject of a number of studies over the last 20 years. In particular we have focused on mitogen activated protein (MAP) kinases, key components of a number of signal transduction pathways. We have recently characterized the three central components of the three MAP kinase cascades present in filamentous fungi deleting Cpkk1, Cpkk2 and Cpkk3, the three MEK genes present in the Cryphonectria parasitica genome. When we attempted to infect through anasthomosis each of the three knock out strains, only the knock out strain of Cpkk2, the yeast Ste7 homologue, involved in mating and filamentous growth, could not be infected. We then proceeded to attempt virus infection through transformation of protoplasts obtained from a Cpkk2 deficient strain using an infectious cDNA clone able to establish virus infection through transformation: in this case a very limited number of strains could be recovered as stable transformants when compared to the efficiency of control transformations with plasmid carrying only the antibiotic marker. Furthermore, transformants carrying actively replicating virus could be isolated only if the marker for selection, Geneticin, was used only for the very initial selection process, and not maintained throughout the growth of the colonies. Furthermore, Cpkk2 isolates that maintained the virus, lost the marker for Geneticin resistance. We therefore unveiled a specific negative interaction among virus infection, presence of Geneticin in the growth media, and lack of Cpkk2 MEK in the fungal host. (literal)
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