N6-adenosine methylation of mRNA integrates multilevel auxin response and ground tissue development in Arabidopsis
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61389030%3A_____%2F23%3A00578511" target="_blank" >RIV/61389030:_____/23:00578511 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/00216224:14740/23:00134766 RIV/00216208:11310/23:10471876 RIV/61989592:15310/23:73623012
Výsledek na webu
<a href="https://doi.org/10.1242/dev.201775" target="_blank" >https://doi.org/10.1242/dev.201775</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1242/dev.201775" target="_blank" >10.1242/dev.201775</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
N6-adenosine methylation of mRNA integrates multilevel auxin response and ground tissue development in Arabidopsis
Popis výsledku v původním jazyce
N6-methyl adenosine (m6A) is a widespread internal mRNA modification impacting the expression of numerous genes. Here, we characterize auxin-related defects among the pleiotropic phenotypes of hypomorphic Arabidopsis thaliana mutants with impaired m6A status and reveal that they show strong resistance to exogenously applied auxin. By combining major published m6A datasets, we propose that among high-confidence target transcripts emerge those encoding the main components required for auxin signaling, including the TIR1/AFB auxin receptors and ARF transcriptional regulators. We also observe subtle changes in endogenous levels of indole-3-acetic acid metabolites in these hypomorphic lines, which correlate with the methylation status of indole-3-acetic acid amidohydrolase transcripts. In addition, we reveal that reduced m6A levels lead to defects in endodermal patterning in the primary root arising from impaired timing of periclinal cell divisions. These defects can be reverted by inhibition of auxin signaling. Together, our data underline that m6A likely affects auxin-dependent processes at multiple levels.
Název v anglickém jazyce
N6-adenosine methylation of mRNA integrates multilevel auxin response and ground tissue development in Arabidopsis
Popis výsledku anglicky
N6-methyl adenosine (m6A) is a widespread internal mRNA modification impacting the expression of numerous genes. Here, we characterize auxin-related defects among the pleiotropic phenotypes of hypomorphic Arabidopsis thaliana mutants with impaired m6A status and reveal that they show strong resistance to exogenously applied auxin. By combining major published m6A datasets, we propose that among high-confidence target transcripts emerge those encoding the main components required for auxin signaling, including the TIR1/AFB auxin receptors and ARF transcriptional regulators. We also observe subtle changes in endogenous levels of indole-3-acetic acid metabolites in these hypomorphic lines, which correlate with the methylation status of indole-3-acetic acid amidohydrolase transcripts. In addition, we reveal that reduced m6A levels lead to defects in endodermal patterning in the primary root arising from impaired timing of periclinal cell divisions. These defects can be reverted by inhibition of auxin signaling. Together, our data underline that m6A likely affects auxin-dependent processes at multiple levels.
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
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2023
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Development
ISSN
0950-1991
e-ISSN
1477-9129
Svazek periodika
150
Číslo periodika v rámci svazku
19
Stát vydavatele periodika
GB - Spojené království Velké Británie a Severního Irska
Počet stran výsledku
11
Strana od-do
dev201775
Kód UT WoS článku
001092309300002
EID výsledku v databázi Scopus
2-s2.0-85174817550