Inositol Trisphosphate-Induced Ca2+ Signaling Modulates Auxin Transport and PIN Polarity
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61389030%3A_____%2F11%3A00360769" target="_blank" >RIV/61389030:_____/11:00360769 - isvavai.cz</a>
Výsledek na webu
<a href="http://dx.doi.org/10.1016/j.devcel.2011.05.013" target="_blank" >http://dx.doi.org/10.1016/j.devcel.2011.05.013</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1016/j.devcel.2011.05.013" target="_blank" >10.1016/j.devcel.2011.05.013</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Inositol Trisphosphate-Induced Ca2+ Signaling Modulates Auxin Transport and PIN Polarity
Popis výsledku v původním jazyce
Directional auxin flow within tissues depends on polar localization of PIN transporters. To explore regulation of PIN-mediated auxin transport, we screened for suppressors of PIN1 overexpression (supo) and identified an inositol polyphosphate 1-phosphatase mutant (supo1), with elevated inositol trisphosphate (InsP3) and cytosolic Ca2+ levels. Increases in InsP3 or Ca2+ levels also suppressed the PIN1 phenotypes and caused defects in basal PIN localization, auxin transport and auxin mediated development.Reductions in InsP3 levels and Ca2+ signaling antagonized the effects of the supo1 mutation and disrupted preferentially apical PIN localization. InsP3 and Ca2+ are evolutionarily conserved second messengers involved in various cellular functions, particularly stress responses. Our findings implicate them as modifiers of cell polarity and polar auxin transport, and highlight a potential integration point through which Ca2+ signaling-related stimuli could influence auxin-mediated develop
Název v anglickém jazyce
Inositol Trisphosphate-Induced Ca2+ Signaling Modulates Auxin Transport and PIN Polarity
Popis výsledku anglicky
Directional auxin flow within tissues depends on polar localization of PIN transporters. To explore regulation of PIN-mediated auxin transport, we screened for suppressors of PIN1 overexpression (supo) and identified an inositol polyphosphate 1-phosphatase mutant (supo1), with elevated inositol trisphosphate (InsP3) and cytosolic Ca2+ levels. Increases in InsP3 or Ca2+ levels also suppressed the PIN1 phenotypes and caused defects in basal PIN localization, auxin transport and auxin mediated development.Reductions in InsP3 levels and Ca2+ signaling antagonized the effects of the supo1 mutation and disrupted preferentially apical PIN localization. InsP3 and Ca2+ are evolutionarily conserved second messengers involved in various cellular functions, particularly stress responses. Our findings implicate them as modifiers of cell polarity and polar auxin transport, and highlight a potential integration point through which Ca2+ signaling-related stimuli could influence auxin-mediated develop
Klasifikace
Druh
J<sub>x</sub> - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)
CEP obor
ED - Fyziologie
OECD FORD obor
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Návaznosti výsledku
Projekt
—
Návaznosti
Z - Vyzkumny zamer (s odkazem do CEZ)
Ostatní
Rok uplatnění
2011
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Developmental Cell
ISSN
1534-5807
e-ISSN
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Svazek periodika
20
Číslo periodika v rámci svazku
6
Stát vydavatele periodika
US - Spojené státy americké
Počet stran výsledku
12
Strana od-do
855-866
Kód UT WoS článku
000291763500013
EID výsledku v databázi Scopus
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