The signaling pathways underlying starvation-induced upregulation of α-mannosidase Ams1 in Saccharomyces cerevisiae

Umekawa, Midori; Ujihara, Masato; Makishima, Kazuki; Yamamoto, Shohei; Takematsu, Hiromu; Wakayama, Mamoru

doi:10.1016/j.bbagen.2016.02.018

Cited by 15 publications

(24 citation statements)

References 27 publications

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“…Gene deletions were performed by a standard PCR-based procedure [17]. A plasmid encoding the GFP-tagged Ams1 with an endogenous promoter (pRS426-Ams1-GFP) was constructed as described previously [16]. For starvation, YP-Glc (1% yeast extract and 2% peptone) or SD-N (0.17% yeast nitrogen base without ammonium sulfate and amino acids, and 2% glucose) were used.…”

Section: Methodsmentioning

confidence: 99%

“…We read out the activity of the TORC1 signaling pathway by means of monitoring the intracellular activity of a-mannosidase (Ams1), since we have previously shown that Ams1 was induced by inactivation of TORC1 [16]. This unicellular model organism is suited for this purpose since yeast cells respond to extracellular nutrients.…”

Section: Edited By Francesc Posasmentioning

confidence: 99%

“…As well as aminopeptidase 1 (Ape1), Ams1 is known to be a substrate for autophagy that is transported from the cytosol into the vacuoles [21][22][23]. Ams1 was upregulated most strikingly by glucose starvation but also upregulated by nitrogen starvation [16]. In conjunction with autophagy, the enzymatic activity of Ams1 was partially enhanced by a proteinase A (Pep4)-dependent processing in the vacuoles [16].…”

Section: Ecm33 Is Required For Suppression Of Ams1 Under the Nutrientmentioning

confidence: 99%

“…Ams1 was upregulated most strikingly by glucose starvation but also upregulated by nitrogen starvation [16]. In conjunction with autophagy, the enzymatic activity of Ams1 was partially enhanced by a proteinase A (Pep4)-dependent processing in the vacuoles [16]. It was suggested that the regulation of Ams1 was conducted by TORC1, synchronized with PKA/Snf1 pathways [16].…”

Section: Ecm33 Is Required For Suppression Of Ams1 Under the Nutrientmentioning

confidence: 99%

“…In conjunction with autophagy, the enzymatic activity of Ams1 was partially enhanced by a proteinase A (Pep4)-dependent processing in the vacuoles [16]. It was suggested that the regulation of Ams1 was conducted by TORC1, synchronized with PKA/Snf1 pathways [16]. It is known that TORC1 is activated in the presence of abundant nutrient, but suppressed by deprivation of either the nitrogen source or the carbon source [3,8,24].…”

Section: Ecm33 Is Required For Suppression Of Ams1 Under the Nutrientmentioning

confidence: 99%

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Ecm33 is a novel factor involved in efficient glucose uptake for nutrition‐responsive TORC1 signaling in yeast

et al. 2017

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Glucose uptake is crucial for providing both an energy source and a signal that regulates cell proliferation. Therefore, it is important to clarify the mechanisms underlying glucose uptake and its transmission to intracellular signaling pathways. In this study, we searched for a novel regulatory factor involved in glucose-induced signaling by using Saccharomyces cerevisiae as a eukaryotic model. Requirement of the extracellular protein Ecm33 in efficient glucose uptake and full activation of the nutrient-responsive TOR kinase complex 1 (TORC1) signaling pathway is shown. Cells lacking Ecm33 elicit a series of starvation-induced pathways even in the presence of extracellular high glucose concentration. This results in delayed cell proliferation, reduced ATP, induction of autophagy, and dephosphorylation of the TORC1 substrates Atg13 and Sch9.

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Section: Methodsmentioning

confidence: 99%

Section: Edited By Francesc Posasmentioning

confidence: 99%

Section: Ecm33 Is Required For Suppression Of Ams1 Under the Nutrientmentioning

confidence: 99%

Section: Ecm33 Is Required For Suppression Of Ams1 Under the Nutrientmentioning

confidence: 99%

Section: Ecm33 Is Required For Suppression Of Ams1 Under the Nutrientmentioning

confidence: 99%

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Ecm33 is a novel factor involved in efficient glucose uptake for nutrition‐responsive TORC1 signaling in yeast

et al. 2017

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Mitotic cyclin Clb4 is required for the intracellular adaptation to glucose starvation in Saccharomyces cerevisiae

et al. 2019

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Edited by Ivan SadowskiCellular homeostasis in response to glucose availability is maintained through the tight coordination of various physiological processes, including cell proliferation, transcription, and metabolism. In this study, we use the budding yeast Saccharomyces cerevisiae to identify proteins implicated in carbon source-dependent modulation of physiological processes. We find that the mitotic cyclin Clb4 is required for optimal regulation of glucose-starvation-responsive pathways through the target of rapamycin complex 1. Cells lacking Clb4 are characterized by dysregulation of autophagy and impaired modulation of cell size. Notably, cell viability after prolonged glucose starvation is severely reduced by disruption of Clb4. We conclude that Clb4, in addition to its function in the cell cycle, plays a role in the intracellular adaptation to glucose starvation.

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Expression and Characterization of a GH38 α-Mannosidase from the Hyperthermophile Pseudothermotoga thermarum

Yan

Nie

et al. 2022

Appl Biochem Biotechnol

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The signaling pathways underlying starvation-induced upregulation of α-mannosidase Ams1 in Saccharomyces cerevisiae

Cited by 15 publications

References 27 publications

Ecm33 is a novel factor involved in efficient glucose uptake for nutrition‐responsive TORC1 signaling in yeast

Ecm33 is a novel factor involved in efficient glucose uptake for nutrition‐responsive TORC1 signaling in yeast

Mitotic cyclin Clb4 is required for the intracellular adaptation to glucose starvation in Saccharomyces cerevisiae

Expression and Characterization of a GH38 α-Mannosidase from the Hyperthermophile Pseudothermotoga thermarum

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