nuclear localization of Yap1p increased tolerance to diamide, but caused hypersensitivity to H2O2. Furthermore, it has been recently published 1692608 that H2O2 and diamide trigger Yap1p nuclear localization differently, therefore they promote distinct antioxidant responses. Further evidence that supports the existence of different antioxidant transcriptional responses yet to be described is that Tsa1p deficiency alters the expression of several Yap1p-targeted genes in the presence of H2O2 without affecting Yap1p nuclear localization. Hence, all these reports suggest 
that alternative mechanisms for the oxidative stress response still to be described may exist, which coordinate Trx2p, Tsa1p, Yap1p, Skn7p, and other putative regulatory proteins. Studies into oxidative stress response regulation in S. cerevisiae have been carried out only with laboratory yeast strains mainly at low H2O2 doses. However, very little is known about the oxidative stress regulation in natural wine yeast strains, which are much more resistant than laboratory strains. Our wine strains studies done under industrial conditions in molasses medium have shown how the TRX2 gene overexpression increases biomass yield under respiratory conditions by not only improving the oxidative stress response, but also by preventing protein damages from carbonylation Amezinium metilsulfate web events. Furthermore, a global transcriptional analysis of wine yeast strain under industrial conditions has demonstrated that TRX2 gene manipulation affects the expression of several oxidative stress response genes during industrial performance. Therefore, the Plasmid pFA6a-13Myc-KanMX6 GCREGPX2-CYC1TATA-lacZ YRETRX2-CYC1TATA-lacZ The autism spectrum disorders are a heterogeneous group of neurodevelopmental disorders defined by impairments in communication and social interactions along with restrictive and repetitive behaviors. An estimated 1 out of 88 individuals in the United States are currently affected with an ASD and the incidence continues to rise. Despite decades of research, we have limited knowledge of the causes of ASD or the risks associated with developing ASD. Recent studies have recognized that a broad range of children with ASD have impairments in several basic physiological processes such as energy generation systems and redox homeostasis. Mitochondrial dysfunction has become increasingly accepted as a major physiological disturbance in ASD. However, the etiology of mitochondrial dysfunction is not known. Indeed, although mitochondrial deoxyribonucleic acid mutations are commonly found in classical mitochondrial disease, such mutations are found in only 23% of ASD children diagnosed with MD. This raises the possibility of acquired mitochondrial dysfunction since mitochondrial damage can result from environmental exposures implicated in ASD such as heavy metals, exhaust fumes, polychlorinated biphenyls or pesticides. Alternatively, mitochondria can be damaged by endogenous stressors associated with ASD such as elevated proinflammatory cytokines resulting from an activated immune system or other conditions associated with oxidative stress. The notion of an acquired mitochondrial disorder is supported by a recent twin study which concluded that the environment contributes a greater percent of the risk of developing autistic 10355733 disorder as compared to genetic factors with these factors contributing about equally for the broader ASD diagnosis. Oxidative stress may be a key link between mitochondrial dysfunction and A nuclear localization of Yap1p increased tolerance to diamide, but caused hypersensitivity to H2O2. Furthermore, it has been recently published that H2O2 and diamide trigger Yap1p nuclear localization differently, therefore they promote distinct antioxidant responses. Further evidence that supports the existence of different antioxidant transcriptional responses yet to be described is that Tsa1p deficiency alters the expression of several Yap1p-targeted genes in the presence of H2O2 without affecting Yap1p nuclear localization. Hence, all these reports suggest that alternative mechanisms for the oxidative stress response still to be described may exist, which coordinate Trx2p, Tsa1p, Yap1p, Skn7p, and other putative regulatory proteins. Studies into oxidative stress response regulation in S. cerevisiae have been carried out only with laboratory yeast strains mainly at low H2O2 doses. However, very little is known about the oxidative stress regulation in natural wine yeast strains, which are much more resistant than laboratory strains. Our wine strains studies done under industrial conditions in molasses medium have shown how the TRX2 gene overexpression increases biomass yield under respiratory conditions by not only improving the oxidative stress response, but also by preventing protein damages from carbonylation events. Furthermore, a global transcriptional analysis of wine yeast strain under industrial conditions has demonstrated that TRX2 gene manipulation affects the expression of several oxidative 7190624 stress response genes during industrial performance. Therefore, the Plasmid pFA6a-13Myc-KanMX6 GCREGPX2-CYC1TATA-lacZ YRETRX2-CYC1TATA-lacZ The autism spectrum disorders are a heterogeneous group of neurodevelopmental disorders defined by impairments in communication and social interactions along with restrictive and repetitive behaviors. An estimated 1 out of 88 individuals in the United States are currently affected with an ASD and the incidence continues to rise. Despite decades of research, we have limited knowledge of the causes of ASD or the risks associated with developing ASD. Recent studies have recognized that a broad range of children with ASD have impairments in several basic physiological processes such as energy generation systems and redox homeostasis. Mitochondrial dysfunction has become increasingly accepted as a major physiological disturbance in ASD. However, the etiology of mitochondrial dysfunction is not known. Indeed, although mitochondrial deoxyribonucleic acid mutations are commonly found in classical mitochondrial disease, such mutations are found in only 23% of ASD children diagnosed with MD. This raises the possibility of acquired mitochondrial dysfunction since mitochondrial damage can result from environmental exposures implicated in ASD such as heavy metals, exhaust fumes, polychlorinated biphenyls or pesticides. Alternatively, mitochondria can be damaged by endogenous stressors associated with ASD such as elevated proinflammatory cytokines resulting from an activated immune system or other conditions associated with oxidative stress. The notion of an acquired mitochondrial disorder is supported by a recent twin study which concluded 1417961 that the environment contributes a greater percent of the risk of developing autistic disorder as compared to genetic factors with these factors contributing about equally for the broader ASD diagnosis. Oxidative stress may be a key link between mitochondrial dysfunction and A
