title: Gene silencing-based disease resistance.
abstract: The definition of a disease is fundamentally difficult, even if one considers only genetically based diseases. In its broadest sense, disease can be defined as any deviation from the norm that results in a physiological disadvantage. Natural selection ensures that the norm for any given species is constantly changing. In addition, some disadvantages are latent and might only manifest under certain environmental conditions. Conversely, an apparent disadvantage can carry a benefit, for example, the disease sickle-cell anemia that is an advantage in malarial areas. Because of the difficulties in giving disease a precise definition, in this review, gene silencing-based disease resistance will be restricted to the description of gene inactivation processes that contribute to maintain the physical fitness of an organism. In this sense, we are concerned with the elimination of invasive nucleic acid expressing. In numerous organisms, a variety of severe diseases are caused by the attack of invasive nucleic acids such as viruses and retroviral or transposable elements. Organisms have developed diverse mechanisms to defend themselves against such attack that include immune responses and apoptosis. Fungi, plants, invertebrates and vertebrates also enlist gene silencing systems to counteract the harmful effects of invasive nucleic acids. In particular, plants that lack interferon and immune responses have established efficient transcriptional and post-transcriptional gene silencing systems. In this review, we describe how plants defend against invasive nucleic acids and focus on the continual evolutionary battle between plants and viruses. In addition, the importance of controlling transposon activity is outlined. Finally, gene silencing-related mechanisms of genomic imprinting and X-chromosome inactivation are discussed in the context of disease resistance.
authors.affiliation: Fraunhofer-Institute for Molecular Biology and Applied Ecology, Am Klopferspitz 18A, 82152 Martinsried, Germany. wassenegger@ime.fraunhofer.de
authors.forename: Michael
authors.initials: M
authors.lastname: Wassenegger
mesh_terms: D000818:Animals; D004303:Dosage Compensation, Genetic; D020868:Gene Silencing; D006801:Humans; D007113:Immunity, Innate / Q000235:genetics*; D010944:Plants / Q000235:genetics / Q000382:microbiology; D034622:RNA Interference