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Genome-wide identification of genes involved in tolerance to various environmental stresses in Saccharomyces cerevisiae

100%

Auesukaree C. , Damnernsawad A. , Kruatrachue M. , Pokethitiyook P. , Boonchird C. , Kaneko Y. , Harashima S.

tom 50

nr 3

301-310

During fermentation, yeast cells are exposed to a number of stresses - such as high alcohol concentration, high osmotic pressure, and temperature fluctuation - so some overlap of mechanisms involved in the response to these stresses has been suggested. To identify the genes required for tolerance to alcohol (ethanol, methanol, and 1-propanol), heat, osmotic stress, and oxidative stress, we performed genome-wide screening by using 4828 yeast deletion mutants. Our screens identified 95, 54, 125, 178, 42, and 30 deletion mutants sensitive to ethanol, methanol, 1-propanol, heat, NaCl, and H₂O₂, respectively. These deleted genes were then classified based on their cellular functions, and cross-sensitivities between stresses were determined. A large number of genes involved in vacuolar H⁺ -ATPase (V-ATPase) function, cytoskeleton biogenesis, and cell wall integrity, were required for tolerance to alcohol, suggesting their protective role against alcohol stress. Our results revealed a partial overlap between genes required for alcohol tolerance and those required for thermotolerance. Genes involved in cell wall integrity and the actin cytoskeleton are required for both alcohol tolerance and thermotolerance, whereas the RNA polymerase II mediator complex seems to be specific to heat tolerance. However, no significant overlap of genes required for osmotic stress and oxidative stress with those required for other stresses was observed. Interestingly, although mitochondrial function is likely involved in tolerance to several stresses, it was found to be less important for thermotolerance. The genes identified in this study should be helpful for future research into the molecular mechanisms of stress response.

Stem cells migrate from the brain to the periphery using lymphatic vessels to sequester stroke-induced inflammation

84%

Kaya X. , Lee J. Y. , Lin P. , Pianta S. , Vale F. , van Loveren H. , Kaneko Y. , Borlongan C. V.

nr Suppl.1

Investigations of stem cell therapy for neurological disorders have primarily focused on the grafted cells’ effects within the local brain tissue. Despite mounting evidence of a massive peripheral inflammatory response accompanying stroke, the ability of intracerebrally transplanted cells to migrate to the periphery and sequester systemic inflammation remains unexplored. We previously reported that intravenously transplanted human bone marrow stem cells (hBMSCs) preferentially migrate to spleen, subsequently abrogating chronic inflammation in stroke. Here, we tested the hypothesis that intracerebrally transplanted stem cells in the brain of adult rats subjected to experimental stroke can migrate to the spleen, a vital organ that confers peripheral inflammation after stroke. Immunofluorescence microscopy revealed stem cells engrafted in the brain, but interestingly a specialized band of stem of cells homed to the spleen via lymphatic vessels, seemingly propelled by inflammatory signals. Mechanism-based in vitro studies using hBMSCs co-cultured with lymphatic endothelial cells or microglia, and treated with TNF-alpha further implicated the key role of the lymphatic system in directing stem cell migration and in dampening inflammation. Altogether, the results suggest a robust therapeutic outcome in stroke can be achieved by targeting the systemic inflammatory response. This study is the first to demonstrate brain‑to‑periphery migration of stem cells, advancing the novel concept of harnessing the lymphatic system in mobilizing stem cells to sequester peripheral inflammation as a brain repair strategy. FINANCIAL SUPPORT: CVB is supported by the National Institutes of Health.