Becerra M, Lombardía L J, González-Siso M I, Rodríguez-Belmonte E, Hauser N C, Cerdán M E
Dpto. Biología Celular y Molecular, Universidad de La Coruña, F. Ciencias, Campus de La Zapateira s/n, La Coruña 15075, Spain.
Comp Funct Genomics. 2003;4(4):366-75. doi: 10.1002/cfg.301.
DNA arrays were used to measure changes in transcript levels as yeast cells responded to temperature shocks. The number of genes upregulated by temperature shifts from 30 to 37 or 45 was correlated with the severity of the stress. Pre-adaptation of cells, by growth at 37 previous to the 45 shift, caused a decrease in the number of genes related to this response. Heat shock also caused downregulation of a set of genes related to metabolism, cell growth and division, transcription, ribosomal proteins, protein synthesis and destination. Probably all of these responses combine to slow down cell growth and division during heat shock, thus saving energy for cell rescue. The presence of putative binding sites for Xbp1p in the promoters of these genes suggests a hypothetical role for this transcriptional repressor, although other mechanisms may be considered. The response to cold shock (4) affected a small number of genes, but the vast majority of those genes induced by exposure to 4 were also induced during heat shock; these genes share in their promoters cis-regulatory elements previously related to other stress responses.
当酵母细胞对温度冲击作出反应时，DNA阵列被用于测量转录水平的变化。温度从30℃转变到37℃或45℃时上调的基因数量与应激的严重程度相关。在45℃转变之前，通过在37℃生长对细胞进行预适应，导致与这种反应相关的基因数量减少。热休克还导致一组与代谢、细胞生长和分裂、转录、核糖体蛋白、蛋白质合成及定位相关的基因下调。可能所有这些反应共同作用，在热休克期间减缓细胞生长和分裂，从而为细胞救援节省能量。这些基因启动子中存在假定的Xbp1p结合位点，表明了这种转录抑制因子的一种假设作用，不过也可能存在其他机制。冷休克（4℃）反应影响了少数基因，但暴露于4℃诱导的绝大多数基因在热休克期间也被诱导；这些基因在其启动子中共享先前与其他应激反应相关的顺式调控元件。
