Gene repression inS. cerevisiae-looking beyond Sir-dependent gene silencing
Authors: Sauty, Safia Mahabub; Shaban, Kholoud; Yankulov, Krassimir
Gene silencing by theSIR(Silent Information Region) family of proteins inS. cerevisiaehas been extensively studied and has served as a founding paradigm for our general understanding of gene repression and its links to histone deacetylation and chromatin structure. In recent years, our understanding of other mechanisms of gene repression inS.cerevisiaewas significantly advanced. In this review, we focus on such Sir-independent mechanisms of gene repression executed by various Histone Deacetylases (HDACs) and Histone Methyl Transferases (HMTs). We focus on the genes regulated by these enzymes and their known mechanisms of action. We describe the cooperation and redundancy between HDACs and HMTs, and their involvement in gene repression by non-coding RNAs or by their non-histone substrates. We also propose models of epigenetic transmission of the chromatin structures produced by these enzymes and discuss these in the context of gene repression phenomena in other organisms. These include the recycling of the epigenetic marks imposed by HMTs or the recycling of the complexes harboring HDACs.
Microorganisms associated to thyroid autoimmunity
Authors: Cuan-Baltazar, Yunam; Soto-Vega, Elena
Autoimmune thyroid diseases are a group of diseases characterized by a dysfunction of the immune system concerning the thyroid gland, associated with hypothyroidism or hyperthyroidism. The thyroid gland auto immunity has been recognized as multifactorial. It has been reported that microorganisms may play a role on the pathogenesis of Hashimoto's thyroiditis and Graves' disease. These could explain the high incidence of the autoimmune thyroid diseases. Helicobacter Pylori (H. pylori) and Hepatitis C virus (HCV) are the microorganisms in which the association with autoimmune thyroid diseases is clearer. The pathophysiologic mechanisms are still not well defined. For H. pylori, molecular mimicry has been the most accepted mechanism. It has been proposed Hepatitis C virus as the trigger of the thyroid autoimmunity by exacerbating the production of thyroid auto-antibodies, while some mention that the real factor that triggers the thyroid autoimmunity is the treatment with Interferon alpha (IFN-alpha) by upregulating MHC class I and inducing ligation of CD40+ cells to thyrocytes. Other microorganisms such as Toxoplasma gondii, Human Immunodeficiency virus, Herpes virus and others have reported information about their association with thyroid autoimmune diseases There are no proposals on how these last microorganisms induce thyroid autoimmunity. There is still a lack of evidence on this topic. Further research must be done to determine the interaction of these microorganisms and the best way to manage these patients.