Buisson N, Labbe-Bois R
Laboratoire de Biochimie des Porphyrines, Institut Jacques Monod, Université Paris 7, 2 place Jussieu, 75251 Paris, France.
J Biol Chem. 1998 Apr 17;273(16):9527-33. doi: 10.1074/jbc.273.16.9527.
The yeast Saccharomyces cerevisiae contains a flavohemoglobin, encoded by the gene YHB1, whose function is unclear. Previous reports presented evidence that its maximal expression requires disruption of mitochondrial respiration and that it plays a role in the response to oxidative stress. We have studied the expression of YHB1 in respiratory deficient cells and in cells exposed to various compounds causing oxidative stress. Several different strains and approaches (spectroscopic detection of the oxygenated form of Yhb1p, beta-galactosidase activity of a YHB1-lacZ fusion, and Northern blot analysis) were used to demonstrate that YHB1 expression and Yhb1p production are not increased by respiration deficiency. YHB1 expression was unchanged in cells challenged with antimycin A or menadione, while it decreased in cells exposed to H2O2, diamide, dithiothreitol, and Cu2+. Transcription of YHB1 is not under the control of the transcriptional factor Yap1p. These results do not support a participation of YHB1 in the genetic response to oxidative stress. We also analyzed the growth phenotypes associated with altered Yhb1p production using YHB1-deleted strains and strains that greatly overproduced Yhb1p. Yhb1p appears to protect cells against the damage caused by Cu2+ and dithiothreitol, while sensitizing them to H2O2. Yhb1p overproduction in a glucose-6-phosphate dehydrogenase-deficient mutant decreased its growth rate. These data indicate that there is a complex relationship(s) between Yhb1p function(s) and cell defense reactions against various stresses.
酿酒酵母含有一种由YHB1基因编码的黄素血红蛋白，其功能尚不清楚。先前的报告提供了证据，表明其最大表达需要破坏线粒体呼吸作用，并且它在对氧化应激的反应中起作用。我们研究了YHB1在呼吸缺陷细胞和暴露于各种引起氧化应激的化合物的细胞中的表达。使用了几种不同的菌株和方法（Yhb1p氧化形式的光谱检测、YHB1-lacZ融合的β-半乳糖苷酶活性以及Northern印迹分析）来证明呼吸缺陷不会增加YHB1的表达和Yhb1p的产生。在用抗霉素A或甲萘醌处理的细胞中，YHB1的表达没有变化，而在暴露于过氧化氢、二酰胺、二硫苏糖醇和铜离子的细胞中，YHB1的表达下降。YHB1的转录不受转录因子Yap1p的控制。这些结果不支持YHB1参与对氧化应激的遗传反应。我们还使用YHB1缺失菌株和大量过量产生Yhb1p的菌株分析了与Yhb1p产生改变相关的生长表型。Yhb1p似乎可以保护细胞免受铜离子和二硫苏糖醇造成的损伤，同时使它们对过氧化氢敏感。在葡萄糖-6-磷酸脱氢酶缺陷型突变体中过量产生Yhb1p会降低其生长速率。这些数据表明，Yhb1p的功能与细胞针对各种应激的防御反应之间存在复杂的关系。
