부산대학교 도서관

The assimilation, incorporation, and metabolism of sulfur is a fundamental process across all domains of life, yet how cells deal with varying sulfur availability is not well understood. We studied an unresolved conundrum of sulfur fixation in yeast, in which organosulfur auxotrophy caused by deletion of the homocysteine synthase Met17p is overcome when cells are inoculated at high cell density. In combining the use of self-establishing metabolically cooperating (SeMeCo) communities with proteomic, genetic, and biochemical approaches, we discovered an uncharacterized gene product YLL058Wp, herein named Hydrogen Sulfide Utilizing-1 (HSU1). Hsu1p acts as a homocysteine synthase and allows the cells to substitute for Met17p by reassimilating hydrosulfide ions leaked from met17Δ cells into O-acetyl-homoserine and forming homocysteine. Our results show that cells can cooperate to achieve sulfur fixation, indicating that the collective properties of microbial communities facilitate their basic metabolic capacity to overcome sulfur limitation. In yeast, Met17p deletion induces the overflow of hydrosulfide ions due to methionine auxotrophy. This study identifies a new H2S utilizing enzyme, Hsu1p, that recycles hydrosulfide and confers a growth advantage under sulfur limitation; Hsu1p allows the cells to overcome methionine auxotrophy when grown in high density, underscoring the importance of cell-cell metabolic interactions. Author summary: Sulfur perturbation activates a dormant hydrogen sulfide fixation route via a novel homocysteine synthase Hsu1p. [ABSTRACT FROM AUTHOR]