Sphingolipid/Pkh1/2-TORC1/Sch9 Signaling Regulates Ribosome Biogenesis in Tunicamycin-Induced Stress Response in Yeast

Yabuki, Yukari; Ikeda, Atsuko; Araki, Misako; Kajiwara, Kentaro; Mizuta, Keiko; Funato, Kouichi

doi:10.1534/genetics.118.301874

Cited by 24 publications

(18 citation statements)

References 67 publications

(95 reference statements)

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“…This is also consistent with the model that tricalbins play a role in preventing the accumulation of toxic lipids such as ceramide, which causes ER stress. It is noteworthy that tunicamycin treatment appears to impair the transport of ceramides between the ER and the Golgi ( Pittet et al., 2006 ; Yabuki et al., 2019 ).…”

Section: Discussionmentioning

confidence: 99%

Tricalbins Are Required for Non-vesicular Ceramide Transport at ER-Golgi Contacts and Modulate Lipid Droplet Biogenesis

et al. 2020

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Lipid composition varies among organelles, and the distinct lipid composition is important for specific functions of each membrane. Lipid transport between organelles, which is critical for the maintenance of membrane lipid composition, occurs by either vesicular or non-vesicular mechanisms. In yeast, ceramide synthesized in the endoplasmic reticulum (ER) is transported to the Golgi apparatus where inositolphosphorylceramide (IPC) is formed. Here we show that a fraction of Tcb3p, a yeast tricalbin protein, localizes to ER-Golgi contact sites. Tcb3p and their homologs Tcb1p and Tcb2p are required for formation of ER-Golgi contacts and non-vesicular ceramide transport. Absence of Tcb1p, Tcb2p, and Tcb3p increases acylceramide synthesis and subsequent lipid droplet (LD) formation. As LD can sequester excess lipids, we propose that tricalbins act as regulators of ceramide transport at ER-Golgi contact sites to help reduce a potentially toxic accumulation of ceramides.

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Section: Discussionmentioning

confidence: 99%

Tricalbins Are Required for Non-vesicular Ceramide Transport at ER-Golgi Contacts and Modulate Lipid Droplet Biogenesis

et al. 2020

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“…Our finding also demonstrated that GAS1 -overexpressing yeast cells displayed significantly the ER stress sensitivity under the low-Tm-concentration stress. One possibility for this result is that Tm, as an N-linked glycosylation inhibitor, can block the glycosylation of the overexpressed Gas1 protein, resulting in the accumulation of misfolded protein within the ER and ultimately leading to cell death [32, 33]. Thus, our findings indicated that Gas1p is involved in regulating ER stress responses.…”

Section: Resultsmentioning

confidence: 81%

GAS1Deficient Enhances UPR Activity inSaccharomyces cerevisiae

Cui

Xia

et al. 2019

BioMed Research International

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Beta-1,3-glucanosyltransferase (Gas1p) plays important roles in cell wall biosynthesis and morphogenesis and has been implicated in DNA damage responses and cell cycle regulation in fungi. Yeast Gas1p has also been reported to participate in endoplasmic reticulum (ER) stress responses. However, the precise roles and molecular mechanisms through which Gas1p affects these responses have yet to be elucidated. In this study, we constructed GAS1-deficient (gas1Δ) and GAS1-overexpressing (GAS1 OE) yeast strains and observed that the gas1Δ strain exhibited a decreased proliferation ability and a shorter replicative lifespan (RLS), as well as enhanced activity of the unfolded protein response (UPR) in the absence of stress. However, under the high-tunicamycin-concentration (an ER stress-inducing agent; 1.0 μg/mL) stress, the gas1Δ yeast cells exhibited an increased proliferation ability compared with the wild-type yeast strain. In addition, our findings demonstrated that IRE1 and HAC1 (two upstream modulators of the UPR) are required for the survival of gas1Δ yeast cells under the tunicamycin stress. On the other hand, we provided evidence that the GAS1 overexpression caused an obvious sensitivity to the low-tunicamycin-concentration (0.25 μg/mL). Collectively, our results indicate that Gas1p plays an important role in the ageing and ER stress responses in yeast.

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“…This protein is a glutamine sensor that acts independently of the GSE/EGO complex to activate TORC1 [ 36 ]. Compelling, TORC1 has been linked to endocytosis [ 37 ], ribosome biogenesis [ 38 ], and the HAP complex [ 39 , 40 ] and therefore TORC1 may represent a second central node in polygodial resistance. The TORC1 node is closely linked to the UBI4 node since ubiquitin was shown to exert a positive effect on TORC1 by preventing degradation of the TORC1 subunit Kog1 under stress conditions [ 41 , 42 ].…”

Section: Resultsmentioning

confidence: 99%

Investigating the Antifungal Mechanism of Action of Polygodial by Phenotypic Screening in Saccharomyces cerevisiae

Kipanga

Demuyser

Vrijdag

et al. 2021

IJMS

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Polygodial is a “hot” peppery-tasting sesquiterpenoid that was first described for its anti-feedant activity against African armyworms. Using the haploid deletion mutant library of Saccharomyces cerevisiae, a genome-wide mutant screen was performed to shed more light on polygodial’s antifungal mechanism of action. We identified 66 deletion strains that were hypersensitive and 47 that were highly resistant to polygodial treatment. Among the hypersensitive strains, an enrichment was found for genes required for vacuolar acidification, amino acid biosynthesis, nucleosome mobilization, the transcription mediator complex, autophagy and vesicular trafficking, while the resistant strains were enriched for genes encoding cytoskeleton-binding proteins, ribosomal proteins, mitochondrial matrix proteins, components of the heme activator protein (HAP) complex, and known regulators of the target of rapamycin complex 1 (TORC1) signaling. WE confirm that polygodial triggers a dose-dependent vacuolar alkalinization and that it increases Ca2+ influx and inhibits glucose-induced Ca2+ signaling. Moreover, we provide evidence suggesting that TORC1 signaling and its protective agent ubiquitin play a central role in polygodial resistance, suggesting that they can be targeted by polygodial either directly or via altered Ca2+ homeostasis.

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Sphingolipid/Pkh1/2-TORC1/Sch9 Signaling Regulates Ribosome Biogenesis in Tunicamycin-Induced Stress Response in Yeast

Cited by 24 publications

References 67 publications

Tricalbins Are Required for Non-vesicular Ceramide Transport at ER-Golgi Contacts and Modulate Lipid Droplet Biogenesis

Tricalbins Are Required for Non-vesicular Ceramide Transport at ER-Golgi Contacts and Modulate Lipid Droplet Biogenesis

GAS1Deficient Enhances UPR Activity inSaccharomyces cerevisiae

Investigating the Antifungal Mechanism of Action of Polygodial by Phenotypic Screening in Saccharomyces cerevisiae

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