Lack of cortical endoplasmic reticulum protein Ist2 alters sodium accumulation in Saccharomyces cerevisiae cells

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F17%3A00474850" target="_blank" >RIV/67985823:_____/17:00474850 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1093/femsyr/fox011" target="_blank" >http://dx.doi.org/10.1093/femsyr/fox011</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1093/femsyr/fox011" target="_blank" >10.1093/femsyr/fox011</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Lack of cortical endoplasmic reticulum protein Ist2 alters sodium accumulation in Saccharomyces cerevisiae cells

Popis výsledku v původním jazyce

The maintenance of intracellular alkali-metal-cation homeostasis is a fundamental property of all living organisms, including the yeast Saccharomyces cerevisiae. Several transport systems are indispensable to ensure proper alkali-metal-cation levels in the yeast cytoplasm and organelles. Ist2 is an endoplasmic reticulum (ER)-resident protein involved, together with other tethering proteins, in the formation of contacts between the plasma and ER membranes. As IST2 gene deletion was shown to influence yeast growth in the presence of sodium, we focused on the roles of Ist2 in the cell response to the presence of various concentrations of alkali metal cations, and its interactions with characterised plasma membrane alkali-metal-cation transporters. Most importantly, we show that, in BY4741 background, the lack of Ist2 results in the accumulation of higher amounts of sodium when the cells are exposed to the presence of this cation, demonstrating the importance of Ist2 for the maintenance of low intracellular levels of toxic sodium. As the function and localisation of alkali-metal-cation exporters is not affected in ist2 Delta cells, IST2 deletion results in an increased non-specific uptake of sodium to cells. Moreover, the deletion of IST2 influences relative cell membrane potential, pH(in) and the growth of cells in the presence of a limiting K+ concentration.

Název v anglickém jazyce

Lack of cortical endoplasmic reticulum protein Ist2 alters sodium accumulation in Saccharomyces cerevisiae cells

Popis výsledku anglicky

The maintenance of intracellular alkali-metal-cation homeostasis is a fundamental property of all living organisms, including the yeast Saccharomyces cerevisiae. Several transport systems are indispensable to ensure proper alkali-metal-cation levels in the yeast cytoplasm and organelles. Ist2 is an endoplasmic reticulum (ER)-resident protein involved, together with other tethering proteins, in the formation of contacts between the plasma and ER membranes. As IST2 gene deletion was shown to influence yeast growth in the presence of sodium, we focused on the roles of Ist2 in the cell response to the presence of various concentrations of alkali metal cations, and its interactions with characterised plasma membrane alkali-metal-cation transporters. Most importantly, we show that, in BY4741 background, the lack of Ist2 results in the accumulation of higher amounts of sodium when the cells are exposed to the presence of this cation, demonstrating the importance of Ist2 for the maintenance of low intracellular levels of toxic sodium. As the function and localisation of alkali-metal-cation exporters is not affected in ist2 Delta cells, IST2 deletion results in an increased non-specific uptake of sodium to cells. Moreover, the deletion of IST2 influences relative cell membrane potential, pH(in) and the growth of cells in the presence of a limiting K+ concentration.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10612 - Mycology

Projekt

<a href="/cs/project/LH14297" target="_blank" >LH14297: Regulace vnitrobuněčného pH a homeostáze kationtů a vápníku a draslíku v pučících kvasinkách</a><br>

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2017

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

FEMS Yeast Research

ISSN

1567-1356

e-ISSN

—

Svazek periodika

17

Číslo periodika v rámci svazku

2

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

11

Strana od-do

—

Kód UT WoS článku

000400577600006

EID výsledku v databázi Scopus

2-s2.0-85019686849