酿酒酵母SCH9基因缺失抑制其H2S代谢

H2S作为NO、CO之后的第三个气体信号分子，在心血管和神经系统方面的显著效果引起了人们的关注。酿酒酵母Sch9同源于人类S6K1，可以调节细胞周期和寿命。一定程度内增加细胞内H2S的浓度和SCH9缺失均可延长动物寿命，同样 H2S和Sch9也参与了热量限制延长寿命的机制。为了研究酿酒酵母SCH9缺失是否影响其H2S代谢，我们用GYY4137和NaHS作为H2S供体，用醋酸铅试纸检测反应体系中H2S含量，以酿酒酵母SCH9缺失型菌株RCD398、RCD399和TS120-2d为研究对象，探究SCH9基因缺失对其H2S代谢的影响。结果发现在SCH9缺失型菌株中，非热量限制和热量限制均下调其H2S的生成，也可下调其对外源H2S的代谢。由此推测酿酒酵母SCH9缺失既可以下调其H2S的生成，也可以下调其对外源H2S的代谢，这对酿酒酵母中H2S代谢的进一步研究奠定了理论基础。

The metabolism of H2S is inbibited by saccharomyces cerevisiae SCH9 gene deletion

Hydrogen sulfide (H2S) is the third endogenous signaling molecule after nitric oxide and carbon monoxide. Attention towards H2S has been increasing due to its significant role in the cardiovascular and nervous systems. Saccharomyces cerevisiae Sch9 is homologous to human S6K1, which regulate cell cycle as well as life span. The SCH9 deletion and limited increase in the intracellular H2S can prolong the lifespan of animals. They both are also involved in the mechanism of caloric restriction to extend life.In order to study whether SCH9 deletion can affect the metabolism of H2S in yeast . GYY4137 and NaHS were used as H2S donors and lead acetate paper was employed for testing H2S in SCH9 deletion strains RCD398, RCD399 and TS120-2d.Results indicated that synthesis of H2S is negatively regulated by SCH9 deletion strains with or without caloric restriction. Similarly, catabolism of H2S were down regulated.Thus we speculate that SCH9 deletion decreased synthesis and catabolism of H2S in yeast, which laid a theoretical foundation for further study of H2S metabolism.