Nitrate signaling promotes plant growth by upregulating gibberellin biosynthesis and destabilization of DELLA proteins
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61389030%3A_____%2F21%3A00553400" target="_blank" >RIV/61389030:_____/21:00553400 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/61989592:15310/21:73617050
Výsledek na webu
<a href="http://doi.org/10.1016/j.cub.2021.09.024" target="_blank" >http://doi.org/10.1016/j.cub.2021.09.024</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1016/j.cub.2021.09.024" target="_blank" >10.1016/j.cub.2021.09.024</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Nitrate signaling promotes plant growth by upregulating gibberellin biosynthesis and destabilization of DELLA proteins
Popis výsledku v původním jazyce
Nitrate, one of the main nitrogen (N) sources for crops, acts as a nutrient and key signaling molecule coordinating gene expression, metabolism, and various growth processes throughout the plant life cycle. It is widely accepted that nitrate-triggered developmental programs cooperate with hormone synthesis and transport to finely adapt plant architecture to N availability. Here, we report that nitrate, acting through its signaling pathway, promotes growth in Arabidopsis and wheat, in part by modulating the accumulation of gibberellin (GA)-regulated DELLA growth repressors. We show that nitrate reduces the abundance of DELLAs by increasing GA contents through activation of GA metabolism gene expression. Consistently, the growth restraint conferred by nitrate deficiency is partially rescued in global-DELLA mutant that lacks all DELLAs. At the cellular level, we show that nitrate enhances both cell proliferation and elongation in a DELLA-dependent andindependent manner, respectively. Our findings establish a connection between nitrate and GA signaling pathways that allow plants to adapt their growth to nitrate availability.
Název v anglickém jazyce
Nitrate signaling promotes plant growth by upregulating gibberellin biosynthesis and destabilization of DELLA proteins
Popis výsledku anglicky
Nitrate, one of the main nitrogen (N) sources for crops, acts as a nutrient and key signaling molecule coordinating gene expression, metabolism, and various growth processes throughout the plant life cycle. It is widely accepted that nitrate-triggered developmental programs cooperate with hormone synthesis and transport to finely adapt plant architecture to N availability. Here, we report that nitrate, acting through its signaling pathway, promotes growth in Arabidopsis and wheat, in part by modulating the accumulation of gibberellin (GA)-regulated DELLA growth repressors. We show that nitrate reduces the abundance of DELLAs by increasing GA contents through activation of GA metabolism gene expression. Consistently, the growth restraint conferred by nitrate deficiency is partially rescued in global-DELLA mutant that lacks all DELLAs. At the cellular level, we show that nitrate enhances both cell proliferation and elongation in a DELLA-dependent andindependent manner, respectively. Our findings establish a connection between nitrate and GA signaling pathways that allow plants to adapt their growth to nitrate availability.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
10611 - Plant sciences, botany
Návaznosti výsledku
Projekt
Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.
Návaznosti
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Ostatní
Rok uplatnění
2021
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Current Biology
ISSN
0960-9822
e-ISSN
1879-0445
Svazek periodika
31
Číslo periodika v rámci svazku
22
Stát vydavatele periodika
GB - Spojené království Velké Británie a Severního Irska
Počet stran výsledku
12
Strana od-do
4971-4982
Kód UT WoS článku
000730117100008
EID výsledku v databázi Scopus
2-s2.0-85119347282