Simultaneous structural replacement of the sphingoid long‐chain base and sterol in budding yeast

Abstract

The basic structures of membrane lipids that compose biomembranes differ among species; i.e., in mammals, the primary structure of long‐chain base (LCB), the common backbone of ceramides and complex sphingolipids, is sphingosine, whereas, in yeast Saccharomyces cerevisiae, it is phytosphingosine, and S. cerevisiae does not have sphingosine. In addition, the sterol, which is coordinately involved in various functions with complex sphingolipids, is cholesterol in mammals, while in yeast it is ergosterol. Previously, it was found that yeast cells are viable when the structure of LCBs is replaced by sphingosine by supplying an exogenous LCB to cells lacking LCB biosynthesis. Here, we characterized yeast cells having sphingosine instead of phytosphingosine (sphingosine cells). Sphingosine cells exhibited a strong growth defect when biosynthesis of ceramides or complex sphingolipids was inhibited, indicating that, in the sphingosine cells, exogenously added sphingosine is required to be further metabolized. The sphingosine cells exhibited hypersensitivity to various environmental stresses and had abnormal plasma membrane and cell wall properties. Furthermore, we also established a method for simultaneous replacement of both LCB and sterol structures with those of mammals (sphingosine/cholesterol cells). The multiple stress hypersensitivity and abnormal plasma membrane and cell wall properties observed in sphingosine cells were also observed in sphingosine/cholesterol cells, suggesting that simultaneous replacement of both LCB and sterol structures with those of mammals cannot prevent these abnormal phenotypes. This is the first study to our knowledge showing that S. cerevisiae can grow even if LCB and sterol structures are simultaneously replaced with mammalian types.

The Plasma Membrane H+ ATPase CsPMA2 Regulates Lipid Droplet Formation, Appressorial Development and Virulence in Colletotrichum siamense

“…Previous studies have shown that there may be an interplay between lipids and PMA1 in fungi. PMA1 is reported to localize in lipid microdomains of the plasma membrane, and studies in Saccharomyces cerevisiae have shown that the efficient function of PMA1 is greatly dependent on sphingolipids [36,37]. However, the relationship between plasma membrane H + -ATPase and LD formation remains unclear.…”

“…PMA1 has been reported to be localized in the lipid microdomains of the plasma membrane, and studies in Saccharomyces cerevisiae have shown that the efficient function of PMA1 is greatly dependent on sphingolipids [27,36]. Abnormally high ergosterol accumulation at the plasma membrane disrupts the structures of lipid rafts, resulting in the mislocalization of PMA1 in cells [15,27,37]. However, the relationship between plasma membrane H + -ATPase and LDs is not fully understood.…”