Loss of tolerance to multiple environmental stresses due to limitation of structural diversity of complex sphingolipids

Koga, Ayano; Takayama, Chihiro; Ishibashi, Yoshihiro; Kono, Yushi; Matsuzaki, Momoko; Tani, Motohiro

doi:10.1091/mbc.e22-04-0117

Cited by 7 publications

(19 citation statements)

References 79 publications

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“…Thus, it is most likely that the hypersensitivity to CFW in SPH cells reflects impairment of cell wall integrity. Yeast cells with loss of structural diversity of complex sphingolipids exhibit hypersensitivity to elevated temperature due to damage to cell walls [21,46]. As compared with PHS cells, SPH cells also show hypersensitivity to 39 °C without rhodamine 6G incorporation efficiency being affected (Figs 4E,L and 5J), supporting the notion of impaired cell wall integrity in SPH cells.…”

Section: Discussionmentioning

confidence: 74%

“…5A). Previously, we found that loss of structural diversity of complex sphingolipids, which causes hypersensitivity to multiple environmental stresses, does not also cause significant change of plasma membrane permeability; however, the loss of diversity increases the permeability under several stress conditions [21]. As compared with PHS cells, SPH cells exhibited hypersensitivity to NaCl, sorbitol, pH 3.5, pH 7.5, sorbic acid, high temperature, SDS, and CFW (Fig.…”

Section: Resultsmentioning

confidence: 87%

“…It has been reported that complex sphingolipids are required for acquisition of tolerance to various environmental stresses [6–8,21,25,26]. Thus, we next examined the differences in various stress sensitivities between PHS and SPH cells.…”

Section: Resultsmentioning

confidence: 99%

“…Disruption of genes was performed by replacing their ORFs with the kanMX4 marker from pFA6a‐kanMX4, the hphNT1 marker from pFA6a‐hphNT1, the natNT2 marker from pFA6a‐natNT2 [59], the natMX4 marker from p4339 (pCRII‐TOPO::natMX4) [60], the URA3 marker from pRS406, or the LEU2 marker from pRS405 [61]. For tagging of the C‐terminus of Pil1 with a yeast enhanced green fluorescent protein (yeGFP) tag, a yeGFP fusion cassette with the kanMX4 marker from pKT127 was introduced immediately upstream of the stop codon of chromosomal PIL1 as described previously [62], and the kanMX4 were replaced with the MET15 marker from p3xFLAG‐CMV‐7.1‐MET15 [21]. Pil1‐yeGFP expressing lcb2∆ lcb4∆ upc2‐1 erg1∆ cells (YKY173) were constructed according to the method of [60].…”

Section: Methodsmentioning

confidence: 99%

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

Kono,

Ishibashi,

Fukuda

et al. 2023

The FEBS Journal

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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.

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Section: Discussionmentioning

confidence: 74%

Section: Resultsmentioning

confidence: 87%

Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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

Kono,

Ishibashi,

Fukuda

et al. 2023

The FEBS Journal

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“…Recently, a high-content microscopy screen identified Cvm1 as a protein located at sites where the membrane of the yeast vacuole (which, it should be recalled is the equivalent of a mammalian lysosome [ 200 , 201 ]) contacts three other organelles: mitochondria; peroxisomes; and, the ER emanating from the nuclear envelope [ 202 ]. Changes in the level of Cvm1 alters the levels of multiple sphingolipid classes, which can reduce the tolerance of yeast cells to various environmental stresses [ 203 ], and the contact sites containing Cvm1 are elevated when sphingolipid production is compromised [ 202 ]. The central segment of Cvm1 (residues 244–558) has a strongly predicted homology to the α–β hydrolase fold.…”

Section: Functions Of Ypk1mentioning

confidence: 99%

TOR complex 2 is a master regulator of plasma membrane homeostasis

Thorner

2022

Biochemical Journal

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As first demonstrated in budding yeast (Saccharomyces cerevisiae), all eukaryotic cells contain two, distinct multi-component protein kinase complexes that each harbor the TOR (Target Of Rapamycin) polypeptide as the catalytic subunit. These ensembles, dubbed TORC1 and TORC2, function as universal, centrally important sensors, integrators, and controllers of eukaryotic cell growth and homeostasis. TORC1, activated on the cytosolic surface of the lysosome (or, in yeast, on the cytosolic surface of the vacuole), has emerged as a primary nutrient sensor that promotes cellular biosynthesis and suppresses autophagy. TORC2, located primarily at the plasma membrane, plays a major role in maintaining the proper levels and bilayer distribution of all plasma membrane components (sphingolipids, glycerophospholipids, sterols, and integral membrane proteins). This article surveys what we have learned about signaling via the TORC2 complex, largely through studies conducted in S. cerevisiae. In this yeast, conditions that challenge plasma membrane integrity can, depending on the nature of the stress, stimulate or inhibit TORC2, resulting in, respectively, up-regulation or down-regulation of the phosphorylation and thus the activity of its essential downstream effector the AGC family protein kinase Ypk1. Through the ensuing effect on the efficiency with which Ypk1 phosphorylates multiple substrates that control diverse processes, membrane homeostasis is maintained. Thus, the major focus here is on TORC2, Ypk1, and the multifarious targets of Ypk1 and how the functions of these substrates are regulated by their Ypk1-mediated phosphorylation, with emphasis on recent advances in our understanding of these processes.

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Identification of plb1 mutation that extends longevity via activating Sty1 MAPK in Schizosaccharomyces pombe

Maekawa,

Matsui,

Okamoto

et al. 2024

Mol Genet Genomics

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Loss of tolerance to multiple environmental stresses due to limitation of structural diversity of complex sphingolipids

Cited by 7 publications

References 79 publications

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

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

TOR complex 2 is a master regulator of plasma membrane homeostasis

Identification of plb1 mutation that extends longevity via activating Sty1 MAPK in Schizosaccharomyces pombe

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