Yeast Colony Survival Depends on Metabolic Adaptation and Cell Differentiation Rather Than on Stress Defense
Yeast Colony Survival Depends on Metabolic Adaptation and Cell Differentiation Rather Than on Stress Defense
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DOI：
10.1074/jbc.m109.022871
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发表时间：
2009-11-20
影响因子：
4.8
通讯作者：
Palkova, Zdena
中科院分区：
文献类型：
--
作者：
Cap, Michal;Vachova, Libuse;Palkova, Zdena
清除活性氧（ROS）的酶对应激和衰老过程中的细胞保护非常重要。这些酶的缺乏导致ROS失衡，导致许多生物体（包括酵母）的各种疾病。与液体培养相比，酵母菌群的适应性取决于其ROS清除能力，本研究表明，酿酒酵母细胞生长在能够氨信号传导的菌落中，使用更广泛的保护策略。而不是维持高水平的抗氧化酶的ROS解毒，殖民地激活替代代谢，防止ROS的生产。因此，细胞溶质超氧化物歧化酶Sod1p缺陷菌株的菌落以与野生型菌落相同的方式发育。它们产生了相当水平的氨，并经历了类似的发育变化（在ROS产生、细胞死亡发生和应激防御酶活性中交替代谢和中心边缘分化的基因表达），并且没有积累抗应激抑制剂。然而，胞质过氧化氢酶Ctt1p的缺乏，带来了殖民地的发育问题，这是在线粒体Sod2p的情况下更加突出。sod2 δ和ctt1 δ集落不能产生氨，不能充分激活交替代谢，不能进行中心边缘分化，但它们不增加ROS水平。这些新的数据表明，菌落疾病并不伴随着ROS爆发，但可能是代谢缺陷的结果，然而，这可能是由早期发育阶段产生的ROS不平衡引起的。Sod2p和ROS的稳态可能参与导致氨信号传导的调节事件。
Enzymes scavenging reactive oxygen species (ROS) are important for cell protection during stress and aging. A deficiency in these enzymes leads to ROS imbalance, causing various disorders in many organisms, including yeast. In contrast to liquid cultures, where fitness of the yeast population depends on its ROS scavenging capability, the present study suggests that Saccharomyces cerevisiae cells growing in colonies capable of ammonia signaling use a broader protective strategy. Instead of maintaining high levels of antioxidant enzymes for ROS detoxification, colonies activate an alternative metabolism that prevents ROS production. Colonies of the strain deficient in cytosolic superoxide dismutase Sod1p thus developed the same way as wild type colonies. They produced comparable levels of ammonia and underwent similar developmental changes (expression of genes of alternative metabolism and center margin differentiation in ROS production, cell death occurrence, and activities of stress defense enzymes) and did not accumulate stress-resistant suppressants. An absence of cytosolic catalase Ctt1p, however, brought colonies developmental problems, which were even more prominent in the absence of mitochondrial Sod2p. sod2 Delta and ctt1 Delta colonies failed in ammonia production and sufficient activation of the alternative metabolism and were incapable of center margin differentiation, but they did not increase ROS levels. These new data indicate that colony disorders are not accompanied by ROS burst but could be a consequence of metabolic defects, which, however, could be elicited by imbalance in ROS produced in early developmental phases. Sod2p and homeostasis of ROS may participate in regulatory events leading to ammonia signaling.