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      Yeast AP-1 like transcription factors (Yap) and stress response: a current overview

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          Abstract

          Yeast adaptation to stress has been extensively studied. It involves large reprogramming of genome expression operated by many, more or less specific, transcription factors. Here, we review our current knowledge on the function of the eight Yap transcription factors (Yap1 to Yap8) in Saccharomyces cerevisiae, which were shown to be involved in various stress responses. More precisely, Yap1 is activated under oxidative stress, Yap2/Cad1 under cadmium, Yap4/Cin5 and Yap6 under osmotic shock, Yap5 under iron overload and Yap8/Arr1 by arsenic compounds. Yap3 and Yap7 seem to be involved in hydroquinone and nitrosative stresses, respectively. The data presented in this article illustrate how much knowledge on the function of these Yap transcription factors is advanced. The evolution of the Yap family and its roles in various pathogenic and non-pathogenic fungal species is discussed in the last section.

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          Most cited references173

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          Living with water stress: evolution of osmolyte systems

          Striking convergent evolution is found in the properties of the organic osmotic solute (osmolyte) systems observed in bacteria, plants, and animals. Polyhydric alcohols, free amino acids and their derivatives, and combinations of urea and methylamines are the three types of osmolyte systems found in all water-stressed organisms except the halobacteria. The selective advantages of the organic osmolyte systems are, first, a compatibility with macromolecular structure and function at high or variable (or both) osmolyte concentrations, and, second, greatly reduced needs for modifying proteins to function in concentrated intracellular solutions. Osmolyte compatibility is proposed to result from the absence of osmolyte interactions with substrates and cofactors, and the nonperturbing or favorable effects of osmolytes on macromolecular-solvent interactions.
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            Metals, toxicity and oxidative stress.

            Metal-induced toxicity and carcinogenicity, with an emphasis on the generation and role of reactive oxygen and nitrogen species, is reviewed. Metal-mediated formation of free radicals causes various modifications to DNA bases, enhanced lipid peroxidation, and altered calcium and sulfhydryl homeostasis. Lipid peroxides, formed by the attack of radicals on polyunsaturated fatty acid residues of phospholipids, can further react with redox metals finally producing mutagenic and carcinogenic malondialdehyde, 4-hydroxynonenal and other exocyclic DNA adducts (etheno and/or propano adducts). Whilst iron (Fe), copper (Cu), chromium (Cr), vanadium (V) and cobalt (Co) undergo redox-cycling reactions, for a second group of metals, mercury (Hg), cadmium (Cd) and nickel (Ni), the primary route for their toxicity is depletion of glutathione and bonding to sulfhydryl groups of proteins. Arsenic (As) is thought to bind directly to critical thiols, however, other mechanisms, involving formation of hydrogen peroxide under physiological conditions, have been proposed. The unifying factor in determining toxicity and carcinogenicity for all these metals is the generation of reactive oxygen and nitrogen species. Common mechanisms involving the Fenton reaction, generation of the superoxide radical and the hydroxyl radical appear to be involved for iron, copper, chromium, vanadium and cobalt primarily associated with mitochondria, microsomes and peroxisomes. However, a recent discovery that the upper limit of "free pools" of copper is far less than a single atom per cell casts serious doubt on the in vivo role of copper in Fenton-like generation of free radicals. Nitric oxide (NO) seems to be involved in arsenite-induced DNA damage and pyrimidine excision inhibition. Various studies have confirmed that metals activate signalling pathways and the carcinogenic effect of metals has been related to activation of mainly redox-sensitive transcription factors, involving NF-kappaB, AP-1 and p53. Antioxidants (both enzymatic and non-enzymatic) provide protection against deleterious metal-mediated free radical attacks. Vitamin E and melatonin can prevent the majority of metal-mediated (iron, copper, cadmium) damage both in vitro systems and in metal-loaded animals. Toxicity studies involving chromium have shown that the protective effect of vitamin E against lipid peroxidation may be associated rather with the level of non-enzymatic antioxidants than the activity of enzymatic antioxidants. However, a very recent epidemiological study has shown that a daily intake of vitamin E of more than 400 IU increases the risk of death and should be avoided. While previous studies have proposed a deleterious pro-oxidant effect of vitamin C (ascorbate) in the presence of iron (or copper), recent results have shown that even in the presence of redox-active iron (or copper) and hydrogen peroxide, ascorbate acts as an antioxidant that prevents lipid peroxidation and does not promote protein oxidation in humans in vitro. Experimental results have also shown a link between vanadium and oxidative stress in the etiology of diabetes. The impact of zinc (Zn) on the immune system, the ability of zinc to act as an antioxidant in order to reduce oxidative stress and the neuroprotective and neurodegenerative role of zinc (and copper) in the etiology of Alzheimer's disease is also discussed. This review summarizes recent findings in the metal-induced formation of free radicals and the role of oxidative stress in the carcinogenicity and toxicity of metals.
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              A thiol peroxidase is an H2O2 receptor and redox-transducer in gene activation.

              The Yap1 transcription factor regulates hydroperoxide homeostasis in S. cerevisiae. Yap1 is activated by oxidation when hydroperoxide levels increase. We show that Yap1 is not directly oxidized by hydroperoxide. We identified the glutathione peroxidase (GPx)-like enzyme Gpx3 as a second component of the pathway, serving the role of sensor and transducer of the hydroperoxide signal to Yap1. When oxidized by H2O2, Gpx3 Cys36 bridges Yap1 Cys598 by a disulfide bond. This intermolecular disulfide bond is then resolved into a Yap1 intramolecular disulfide bond, the activated form of the regulator. Thioredoxin turns off the pathway by reducing both sensor and regulator. These data reveal a redox-signaling function for a GPx-like enzyme and elucidate a eukaryotic hydroperoxide-sensing mechanism. Gpx3 is thus a hydroperoxide receptor and redox-transducer.
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                Author and article information

                Journal
                Microb Cell
                Microb Cell
                Microb Cell
                Microb Cell
                Microbial Cell
                Shared Science Publishers OG
                2311-2638
                28 May 2019
                03 June 2019
                : 6
                : 6
                : 267-285
                Affiliations
                [1 ]Instituto de Tecnologia Química e Biológica Anónio Xavier, Universidade Nova de Lisboa, Avenida da República, EAN, Oeiras 2781-901, Oeiras, Portugal.
                [2 ]Sorbonne Université, CNRS, Institut de Biologie Paris-Seine, Laboratory of Computational and Quantitative Biology, F-75005, Paris, France.
                Author notes
                * Corresponding Author: C. Rodrigues-Pousada, Instituto de Tecnologia Química e Biológica Anónio Xavier, Universidade Nova de Lisboa, Avenida da República, EAN, Oeiras 2781-901, Oeiras, Portugal; E-mail: claudina@ 123456itqb.unl.pt

                Conflict of interest: The authors have no conflict of interest to declare.

                Please cite this article as: Claudina Rodrigues-Pousada, Frédéric Devaux, Soraia M. Caetano, Catarina Pimentel, Sofia da Silva, Ana Carolina Cordeiro and Catarina Amaral ( 2019). Yeast AP-1 like transcription factors (Yap) and stress response: a current overview. Microbial Cell 6(6): 267-285. doi: 10.15698/mic2019.06.679

                Article
                MIC0179E110
                10.15698/mic2019.06.679
                6545440
                31172012
                f0ff9df8-fc5d-40f6-8bd5-d05582271ab5
                Copyright @ 2019

                This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduction in any medium, provided the original author and source are acknowledged.

                History
                : 24 January 2019
                : 23 April 2019
                : 09 May 2019
                Funding
                The authors are indebted to Professor Cecília Arraiano for critical reading the manuscript.
                This work was financially supported by the Project LISBOA01-0145-FEDER-007660 (Microbiologia Molecular, Estrutural e Celular, MOSTMICRO) funded by FEDER funds through COMPETE2020 – Programa Operacional Competitividade e Internacionalização (POCI) given to CRP and of “Fundação para a Ciência e a Tecnologia” (FCT) (IF/00124/2015 to C.P) and was financially supported by grants to SC and to A.G.C for fellowships (036/BI/2018, SFRH/BD/118866/2016) respectively. The work of FD is funded by the Agence Nationale pour la Recherche (CANDIHUB project, grant number ANR-14-CE14-0018-02 and STRUDYEV project, grant number ANR-10-JCJC-1603).
                Categories
                Review
                Yeast
                Yap Factors
                Cis-Elements
                Bzip
                Stress

                yeast,yap factors,cis-elements,bzip,stress
                yeast, yap factors, cis-elements, bzip, stress

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