p38-MAPK-mediated translation regulation during early blastocyst development is required for primitive endoderm differentiation in mice

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F60076658%3A12310%2F21%3A43903660" target="_blank" >RIV/60076658:12310/21:43903660 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/67985904:_____/21:00543951 RIV/00216208:11310/21:10438172 RIV/00216224:14740/21:00123879

Výsledek na webu

<a href="https://www.nature.com/articles/s42003-021-02290-z" target="_blank" >https://www.nature.com/articles/s42003-021-02290-z</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1038/s42003-021-02290-z" target="_blank" >10.1038/s42003-021-02290-z</a>

Jazyk výsledku

angličtina

Název v původním jazyce

p38-MAPK-mediated translation regulation during early blastocyst development is required for primitive endoderm differentiation in mice

Popis výsledku v původním jazyce

Successful specification of the two mouse blastocyst inner cell mass (ICM) lineages (the primitive endoderm (PrE) and epiblast) is a prerequisite for continued development and requires active fibroblast growth factor 4 (FGF4) signaling. Previously, we identified a role for p38 mitogen-activated protein kinases (p38-MAPKs) during PrE differentiation, but the underlying mechanisms have remained unresolved. Here, we report an early blastocyst window of p38-MAPK activity that is required to regulate ribosome-related gene expression, rRNA precursor processing, polysome formation and protein translation. We show that p38-MAPK inhibition-induced PrE phenotypes can be partially rescued by activating the translational regulator mTOR. However, similar PrE phenotypes associated with extracellular signal-regulated kinase (ERK) pathway inhibition targeting active FGF4 signaling are not affected by mTOR activation. These data indicate a specific role for p38-MAPKs in providing a permissive translational environment during mouse blastocyst PrE differentiation that is distinct from classically reported FGF4-based mechanisms. Bora et al. show that an early blastocyst window of p38-MAPK activity regulates ribosome-related gene expression, rRNA precursor processing, polysome formation, and protein translation. This study suggests a distinct role of p38-MAPKs for providing a permissive translational environment during mouse blastocyst primitive endoderm differentiation.

Název v anglickém jazyce

p38-MAPK-mediated translation regulation during early blastocyst development is required for primitive endoderm differentiation in mice

Popis výsledku anglicky

Successful specification of the two mouse blastocyst inner cell mass (ICM) lineages (the primitive endoderm (PrE) and epiblast) is a prerequisite for continued development and requires active fibroblast growth factor 4 (FGF4) signaling. Previously, we identified a role for p38 mitogen-activated protein kinases (p38-MAPKs) during PrE differentiation, but the underlying mechanisms have remained unresolved. Here, we report an early blastocyst window of p38-MAPK activity that is required to regulate ribosome-related gene expression, rRNA precursor processing, polysome formation and protein translation. We show that p38-MAPK inhibition-induced PrE phenotypes can be partially rescued by activating the translational regulator mTOR. However, similar PrE phenotypes associated with extracellular signal-regulated kinase (ERK) pathway inhibition targeting active FGF4 signaling are not affected by mTOR activation. These data indicate a specific role for p38-MAPKs in providing a permissive translational environment during mouse blastocyst PrE differentiation that is distinct from classically reported FGF4-based mechanisms. Bora et al. show that an early blastocyst window of p38-MAPK activity regulates ribosome-related gene expression, rRNA precursor processing, polysome formation, and protein translation. This study suggests a distinct role of p38-MAPKs for providing a permissive translational environment during mouse blastocyst primitive endoderm differentiation.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10608 - Biochemistry and molecular biology

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

S - Specificky vyzkum na vysokych skolach

Rok uplatnění

2021

Kód důvěrnosti údajů

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

Název periodika

Communications Biology

ISSN

2399-3642

e-ISSN

—

Svazek periodika

4

Číslo periodika v rámci svazku

1

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

19

Strana od-do

—

Kód UT WoS článku

000668739100001

EID výsledku v databázi Scopus

2-s2.0-85111784798