Yeast osmoregulation – glycerol still in pole position

Blomberg, Anders

doi:10.1093/femsyr/foac035

Cited by 33 publications

(34 citation statements)

References 131 publications

(200 reference statements)

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“…In particular, the determinant role of mitochondria in osmotic stress has been highlighted, although the molecular details are far from being elucidated [ 14 , 15 , 16 ]. Recently, we reported that the RTG pathway acts downstream of HOG1 , the master regulator of osmostress response, and sustains mitochondrial respiratory capacity upon salt stress [ 13 , 17 , 18 ].…”

Section: Introductionmentioning

confidence: 99%

Inactivation of HAP4 Accelerates RTG-Dependent Osmoadaptation in Saccharomyces cerevisiae

Noia

Scarcia

Agrimi

et al. 2023

IJMS

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Mitochondrial RTG (an acronym for ReTroGrade) signaling plays a cytoprotective role under various intracellular or environmental stresses. We have previously shown its contribution to osmoadaptation and capacity to sustain mitochondrial respiration in yeast. Here, we studied the interplay between RTG2, the main positive regulator of the RTG pathway, and HAP4, encoding the catalytic subunit of the Hap2-5 complex required for the expression of many mitochondrial proteins that function in the tricarboxylic acid (TCA) cycle and electron transport, upon osmotic stress. Cell growth features, mitochondrial respiratory competence, retrograde signaling activation, and TCA cycle gene expression were comparatively evaluated in wild type and mutant cells in the presence and in the absence of salt stress. We showed that the inactivation of HAP4 improved the kinetics of osmoadaptation by eliciting both the activation of retrograde signaling and the upregulation of three TCA cycle genes: citrate synthase 1 (CIT1), aconitase 1 (ACO1), and isocitrate dehydrogenase 1 (IDH1). Interestingly, their increased expression was mostly dependent on RTG2. Impaired respiratory competence in the HAP4 mutant does not affect its faster adaptive response to stress. These findings indicate that the involvement of the RTG pathway in osmostress is fostered in a cellular context of constitutively reduced respiratory capacity. Moreover, it is evident that the RTG pathway mediates peroxisomes–mitochondria communication by modulating the metabolic function of mitochondria in osmoadaptation.

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Section: Introductionmentioning

confidence: 99%

Inactivation of HAP4 Accelerates RTG-Dependent Osmoadaptation in Saccharomyces cerevisiae

Noia

Scarcia

Agrimi

et al. 2023

IJMS

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“…Under hyperosmotic conditions, yeast cells synthesize or retain high concentrations of glycerol to maintain their osmotic balance (Blomberg, 2022, de Nadal & Posas, 2022, Hohmann, 2002). Intracellular glycerol concentration is partially regulated by Fps1, an aquaglyceroporin on the plasma membrane.…”

Section: Resultsmentioning

confidence: 99%

The CWI pathway is activated through high hydrostatic pressure, enhancing glycerol efflux via the aquaglyceroporin Fps1 inSaccharomyces cerevisiae

Mochizuki

Tanigawa

Shindo

et al. 2022

Preprint

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The fungal cell wall is the first barrier against diverse external stresses, such as high hydrostatic pressure. This study explores the roles of osmoregulation and the cell wall integrity (CWI) pathway in response to the high pressure in the yeast Saccharomyces cerevisiae. We demonstrate the roles of the transmembrane mechanosensor Wsc1 and aquaglyceroporin Fps1 in an underlying protective mechanism to avoid cellular rupture under high pressure. The promotion of water influx into cells at 25 MPa, as evident by an increase in cell volume and a loss of the plasma membrane eisosome structure, promotes the activation of Wsc1, an activator of the CWI pathway. The downstream mitogen-activated protein kinase Slt2 was hyperphosphorylated at 25 MPa. Glycerol efflux increases via Fps1 phosphorylation, which is initiated by downstream components of the CWI pathway, and contributes to the reduction in intracellular osmolarity under high pressure. Herein, the elucidation of a cellular pathway that is used as a protective mechanism against high pressure could potentially be translated to mammalian cells and could help to understand cellular mechanosensation and adaptation.

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“…There are roughly 570 genes that respond to increased osmolarity in a Hog1-dependent manner, however, only a subset of those (32 genes) appears to be fully Hog1-dependent [ 29 , 30 ]. Examining the published expression changes upon caffeine addition [ 5 ] ( https://www.ncbi.nlm.nih.gov/sites/GDSbrowser?acc=GDS2914 ) we found that fully Hog1-dependent genes like STL1, TKL2, GRE2, DAK1 and PGM2 do not respond to caffeine.…”

Section: Discussionmentioning

confidence: 99%

Caffeine activates HOG-signalling and inhibits pseudohyphal growth in Saccharomyces cerevisiae

Elhasi

Blomberg

2023

BMC Res Notes

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Objective Caffeine has a wide range of effects in humans and other organisms. Caffeine activates p38 MAPK, the human homolog to the Hog1 protein that orchestrates the high-osmolarity glycerol (HOG) response to osmotic stress in the yeast Saccharomyces cerevisiae. Caffeine has also been used as an inducer of cell-wall stress in yeast via its activation of the Pkc1-mediated cell wall integrity (CWI) pathway. In this study, using immunodetection of phosphorylated Hog1, microscopy to score nuclear localisation of GFP-tagged Hog1 and a pseudohyphal growth assays, the effect of caffeine on the HOG-pathway and filamentous growth in yeast was studied. Results It was found that caffeine causes rapid, strong and transient Hog1 dual phosphorylation with statistically significant increases at 20, 30 and 40 mM caffeine. In response to caffeine treatment Hog1 was also rapidly localized to the nucleus, supporting the caffeine-induced phosphorylation and activation of Hog1. We also found that caffeine inhibited the pseudohyphal/filamentous growth in diploid cells, but had no effect on invasive growth in haploids. Our data thus highlights that the HOG signalling pathway is activated by caffeine, which has implications for interpreting caffeine responses in yeast and fungi.

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Yeast osmoregulation – glycerol still in pole position

Cited by 33 publications

References 131 publications

Inactivation of HAP4 Accelerates RTG-Dependent Osmoadaptation in Saccharomyces cerevisiae

Inactivation of HAP4 Accelerates RTG-Dependent Osmoadaptation in Saccharomyces cerevisiae

The CWI pathway is activated through high hydrostatic pressure, enhancing glycerol efflux via the aquaglyceroporin Fps1 inSaccharomyces cerevisiae

Caffeine activates HOG-signalling and inhibits pseudohyphal growth in Saccharomyces cerevisiae

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