Hydrogen sulfide (H2S) is recognized as a neuromodulator as well as neuroprotectant in the brain. H2S can be produced from cysteine by enzymes such as cystathionine beta-synthase. However, a mechanism for releasing H2S under physiologic conditions has not been identified. Here we show that H2S is released from bound sulfur, an intracellular store of sulfur, in neurons and astrocytes of mice and rats in the presence of physiologic concentrations of endogenous reducing substances glutathione and cysteine. The highest pH to release H2S from another sulfur store, acid-labile sulfur, which is localized mainly in mitochondria, is 5.4. Because mitochondria are not in the acidic condition, acid-labile sulfur may not be a physiologic source of H2S. Free H2S is immediately absorbed and stored as bound sulfur. Our novel method, using silver particles to measure free H2S, shows that free H2S is maintained at a low level in basal conditions. Alkalinization of the cytoplasm is required for effective release of H2S from bound sulfur, and this condition is achieved in astrocytes by the high concentrations of extracellular K+ that are normally present when nearby neurons are excited. These data present a new perspective on the regulation of H2S in the brain.
Some strains of Saccharomyces cerevisiae form a biofilm called a "flor" on the surface of wine after ethanolic fermentation, but the molecular mechanism of flor formation by the wild-type flor strain involved in wine making is not clear. Previously, we found that expression of the C-terminally truncated form of NRG1 (NRG1(1-470)) on a multicopy plasmid increases the hydrophobicity of the cell surface, conferring flor formation on the non-flor laboratory strain. Here we show that in Ar5-H12, a wild-type flor haploid strain, flor formation is regulated by NRG1(1-470). Moreover, the disruptant of the wild-type flor diploid strain (Deltaflo11/Deltaflo11) show a weak ability to form the flor. The expression of FLO11 is always high in the wild-type flor strain, regardless of carbon source. Thus FLO11 is primary factor for wild-type flor strains. Furthermore, the disruptant (Deltaflo11) shows lower hydrophobicity of cell surface than the wild type. However, the hydrophobicity of the wild-type flor strains grown in ethanol medium was much higher than those grown in glucose medium. These results indicate that cell surface hydrophobicity is closely related to flor formation in wild-type flor yeasts.
The flor strains of Saccharomyces cerevisiae form a flor on the surface of wine after alcoholic fermentation. High hydrophobicity of the cell surface is suggested to be important for flor formation by the flor wine yeasts. However, the molecular mechanism of flor formation is not clear. We found that expression of C‐terminal deleted NRG1 lacking its two C2H2 zinc finger motifs (NRG11–470) on the multicopy plasmid conferred the ability to form a flor to a non‐flor laboratory strain. The cell surface hydrophobicity of NRG11–470 was higher than of the non‐flor strain. Disruption of the Nrg1p‐repressed gene FLO11, which encodes a cell surface glycoprotein that functions as a flocculin or an adhesin, abolished flor formation. Moreover, expression of FLO11 on a multicopy plasmid could also cause flor formation. These results indicate that FLO11 is essential for flor formation by NRG11–470. In addition, the results suggest that the C‐terminal truncated form of Nrg1p exerts a dominant negative effect on FLO11 repression, resulting in FLO11 expression and, thus, flor formation.
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