Endosomal Na+ (K+)/H+ Exchanger Nhx1/Vps44 Functions Independently and Downstream of Multivesicular Body Formation

Kallay, Laura; Brett, Christopher L.; Tukaye, Deepali N.; Wemmer, Megan; Chyou, Anthony; Odorizzi, Greg; Rao, Rajini

doi:10.1074/jbc.m111.282319

Cited by 17 publications

(18 citation statements)

References 59 publications

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“…A number of screens have identified sphingolipid mutants only with increased sensitivity to salt stress, and none of the strains showed decrease sensitivity. The lag1 Δ, lcb4 Δ, csg1 Δ, csh1 Δ, elo2 Δ, ifa38 Δ, faa3 Δ (Kallay et al, 2011), faa1 Δ (deleted in the fatty acid importers/activators FAA3 and FAA1), ipt1 Δ (Giaever et al, 2002; Kallay et al, 2011), scs7 Δ (Giaever et al, 2002), isc1 Δ (Betz et al, 2002; Giaever et al, 2002), fas1 Δ (de Jesus Ferreira et al, 2001), sur2 Δ (Barreto et al, 2011) show sensitivity to NaCl, KCl and/or LiCl.…”

Section: Phenotypes Of the Yeast Sphingolipid Pathwaymentioning

confidence: 99%

The yeast sphingolipid signaling landscape

Montefusco

Matmati

Hannun

2014

Chemistry and Physics of Lipids

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Sphingolipids are recognized as signaling mediators in a growing number of pathways, and represent potential targets to address many diseases. The study of sphingolipid signaling in yeast has created a number of breakthroughs in the field, and has the potential to lead future advances. The aim of this article is to provide an inclusive view of two major frontiers in yeast sphingolipid signaling. In the first section, several key studies in the field of sphingolipidomics are consolidated to create a yeast sphingolipidome that ranks nearly all known sphingolipid species by their level in a resting yeast cell. The second section presents an overview of most known phenotypes identified for sphingolipid gene mutants, presented with the intention of illuminating not yet discovered connections outside and inside of the field.

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Section: Phenotypes Of the Yeast Sphingolipid Pathwaymentioning

confidence: 99%

The yeast sphingolipid signaling landscape

Montefusco

Matmati

Hannun

2014

Chemistry and Physics of Lipids

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“…nxh1D cells display growth defects in high salt or low pH conditions, and a decrease in intracellular pH (Nass et al 1997;Brett et al 2005). However, Nhx1 was also identified in a screen for mutants with vacuolar protein sorting defects (Bowers et al 2000), and its role in determining the pH of endosomal compartments is critical to protein trafficking, where it may regulate the fusion of these compartments (Qiu and Fratti 2010;Kallay et al 2011;Kojima et al 2012).…”

Section: Alkali Metal Cation Transport In Intracellular Compartmentsmentioning

confidence: 99%

Regulation of Cation Balance inSaccharomyces cerevisiae

2013

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All living organisms require nutrient minerals for growth and have developed mechanisms to acquire, utilize, and store nutrient minerals effectively. In the aqueous cellular environment, these elements exist as charged ions that, together with protons and hydroxide ions, facilitate biochemical reactions and establish the electrochemical gradients across membranes that drive cellular processes such as transport and ATP synthesis. Metal ions serve as essential enzyme cofactors and perform both structural and signaling roles within cells. However, because these ions can also be toxic, cells have developed sophisticated homeostatic mechanisms to regulate their levels and avoid toxicity. Studies in Saccharomyces cerevisiae have characterized many of the gene products and processes responsible for acquiring, utilizing, storing, and regulating levels of these ions. Findings in this model organism have often allowed the corresponding machinery in humans to be identified and have provided insights into diseases that result from defects in ion homeostasis. This review summarizes our current understanding of how cation balance is achieved and modulated in baker's yeast. Control of intracellular pH is discussed, as well as uptake, storage, and efflux mechanisms for the alkali metal cations, Na + and K + , the divalent cations, Ca 2+ and Mg 2+ , and the trace metal ions, Fe 2+ , Zn 2+ , Cu 2+ , and Mn 2+ . Signal transduction pathways that are regulated by pH and Ca 2+ are reviewed, as well as the mechanisms that allow cells to maintain appropriate intracellular cation concentrations when challenged by extreme conditions, i.e., either limited availability or toxic levels in the environment. TABLE OF CONTENTS Abstract 677Introduction 678

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“…Furthermore, in embryos nhx5 nhx6 mutants have defects in processing and transport of seed storage proteins to the vacuole (Ashnest et al, 2015; Reguera et al, 2015). Similar vacuolar trafficking defects have been described in yeast, with the knockout of the single endosomal nhx1 gene causing altered CPY secretion, delayed vacuolar trafficking, and defects in late endosome/ multi-vesicular body (LE/MVB) formation and sorting (Bowers et al, 2000; Brett et al, 2005a; Kallay et al, 2011; Mitsui et al, 2011). Furthermore, RNAi silencing of mammalian endosomal orthologs NHE6 and NHE8 leads to disruptions in endosome trafficking and recycling (Lawrence et al, 2010; Ohgaki et al, 2010), demonstrating that eukaryotic endosomal NHXs have a conserved role in subcellular protein trafficking and recycling.…”

Section: Introductionmentioning

confidence: 54%

NHX-type Na⁺(K⁺)/H⁺ antiporter activity is required for endomembrane trafficking and ion homeostasis in Arabidopsis thaliana

Dragwidge

Scholl

Schumacher

et al. 2018

Preprint

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Here we show through genetic, pharmacological, and live-cell imaging approaches that nhx5 31 nhx6 double knockouts have defects in Golgi and TGN/EE motility, protein recycling at the 32 TGN/EE, but not the secretion of transmembrane proteins. Furthermore, we report that NHX5 33 and NHX6 are required for a novel mechanism of osmotic swelling of late endosomes induced 34 by treatment with the phosphatidylinositol 3/4-kinase inhibitor wortmannin. This wortmannin 35 swelling-insensitive phenotype appears linked to the insensitivity of nhx5 nhx6 TGN/EE to 36 swelling induced with the monovalent cation ionophore monensin, and suggests that NHX5 37 and NHX6 are required for maintaining endosomal cation homeostasis. Lastly, we report that 38 the distal region of the cytosolic tail of NHX6 is required for mediating NHX6 localisation to 39 late endosomes, but does not appear to be essential for NHX6 function. 40

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Endosomal Na+ (K+)/H+ Exchanger Nhx1/Vps44 Functions Independently and Downstream of Multivesicular Body Formation

Cited by 17 publications

References 59 publications

The yeast sphingolipid signaling landscape

The yeast sphingolipid signaling landscape

Regulation of Cation Balance inSaccharomyces cerevisiae

NHX-type Na⁺(K⁺)/H⁺ antiporter activity is required for endomembrane trafficking and ion homeostasis in Arabidopsis thaliana

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Endosomal Na+ (K+)/H+ Exchanger Nhx1/Vps44 Functions Independently and Downstream of Multivesicular Body Formation

Cited by 17 publications

References 59 publications

The yeast sphingolipid signaling landscape

The yeast sphingolipid signaling landscape

Regulation of Cation Balance inSaccharomyces cerevisiae

NHX-type Na+(K+)/H+ antiporter activity is required for endomembrane trafficking and ion homeostasis in Arabidopsis thaliana

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Product

Resources

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NHX-type Na⁺(K⁺)/H⁺ antiporter activity is required for endomembrane trafficking and ion homeostasis in Arabidopsis thaliana