Mensonides Femke I C, Brul Stanley, Klis Frans M, Hellingwerf Klaas J, Teixeira de Mattos M Joost
Swammerdam Institute of Life Sciences, Department of Molecular Microbial Physiology, University of Amsterdam, Nieuwe Achtergracht 166, 1018 WV Amsterdam, The Netherlands.
Appl Environ Microbiol. 2005 Aug;71(8):4531-8. doi: 10.1128/AEM.71.8.4531-4538.2005.
This paper reports on physiological and molecular responses of Saccharomyces cerevisiae to heat stress conditions. We observed that within a very narrow range of culture temperatures, a shift from exponential growth to growth arrest and ultimately to cell death occurred. A detailed analysis was carried out of the accumulation of trehalose and the activation of the protein kinase C1 (PKC1) (cell integrity) pathway in both glucose- and ethanol-grown cells upon temperature upshifts within this narrow range of growth temperatures. It was observed that the PKC1 pathway was hardly activated in a tps1 mutant that is unable to accumulate any trehalose. Furthermore, it was observed that an increase of the extracellular osmolarity during a continuous heat stress prevented the activation of the pathway. The results of these analyses support our hypothesis that under heat stress conditions the activation of the PKC1 pathway is triggered by an increase in intracellular osmolarity, due to the accumulation of trehalose, rather than by the increase in temperature as such.
本文报道了酿酒酵母对热应激条件的生理和分子反应。我们观察到，在非常狭窄的培养温度范围内，会发生从指数生长到生长停滞并最终导致细胞死亡的转变。针对在此狭窄生长温度范围内温度升高时，葡萄糖培养和乙醇培养的细胞中海藻糖的积累以及蛋白激酶C1（PKC1）（细胞完整性）途径的激活进行了详细分析。结果发现，在无法积累任何海藻糖的tps1突变体中，PKC1途径几乎未被激活。此外，还观察到在持续热应激期间细胞外渗透压的增加会阻止该途径的激活。这些分析结果支持了我们的假设，即在热应激条件下，PKC1途径的激活是由海藻糖积累导致的细胞内渗透压升高触发的，而非温度本身的升高。
