Characterization of a new Helicoverpa armigera nucleopolyhedrovirus variant causing epizootic on a previously unreported host, Helicoverpa gelotopoeon (Lepidoptera: Noctuidae)
JOURNAL OF INVERTEBRATE PATHOLOGY
Authors: Ferrelli, M. L.; Taibo, C.; Fichetti, P.; Sciocco-Cap, A.; Arneodo, J. D.
Abstract
This paper reports the first biological and molecular characterization of a nucleopolyhedrovirus isolated from the soybean and cotton pest Helicoverpa gelotopoeon. Studies were performed following a virus outbreak in a rearing facility and in wild H. gelotopoeon populations in Cordoba, Argentina. Host identity was corroborated by partial sequencing of the COI gene. Scanning electron microscope observations of purified OBs revealed their polyhedral morphology and an average diameter of 0.89 +/- 0.141 mu m. Ultrathin sections of infected larvae examined by transmission electron microscopy showed the intranuclear occurrence of polyhedra and virus particles in fat body cells. Nucleocapsids were singly enveloped. Phylogenetic analysis of lef-8, lef-9, polh, orf5/5b and hr3-orf62 viral sequences identified this new NPV isolate (hereafter HegeSNPV) as a variant of Helicoverpa armigera nucleopolyhedrovirus (HearNPV). Furthermore, HegeSNPV was closely related to the so-called "HzSNPV Group" within HearNPV, although having particular characteristics. (C) 2016 Elsevier Inc. All rights reserved.
Adaptive upregulation of DNA repair genes following benzo(a)pyrene diol epoxide protects against cell death at the expense of mutations
NUCLEIC ACIDS RESEARCH
Authors: Christmann, Markus; Boisseau, Catherine; Kitzinger, Rebekka; Berac, Christian; Allmann, Sebastian; Sommer, Tina; Aasland, Dorthe; Kaina, Bernd; Tomicic, Maja T.
Abstract
A coordinated and faithful DNA damage response is of central importance for maintaining genomic integrity and survival. Here, we show that exposure of human cells to benzo(a)pyrene 9,10-diol-7,8-epoxide (BPDE), the active metabolite of benzo(a)pyrene (B(a)P), which represents a most important carcinogen formed during food preparation at high temperature, smoking and by incomplete combustion processes, causes a prompt and sustained upregulation of the DNA repair genes DDB2, XPC, XPF, XPG and POLH. Induction of these repair factors on RNA and protein level enhanced the removal of BPDE adducts from DNA and protected cells against subsequent BPDE exposure. However, through the induction of POLH the mutation frequency in the surviving cells was enhanced. Activation of these adaptive DNA repair genes was also observed upon B(a) P treatment of MCF7 cells and in buccal cells of human volunteers after cigarette smoking. Our data provide a rational basis for an adaptive response to polycyclic aromatic hydrocarbons, which occurs however at the expense of mutations that may drive cancer formation.
COA
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