CHK1-CDC25A-CDK1 regulate cell cycle progression and protect genome integrity in early mouse embryos

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985904%3A_____%2F23%3A00576852" target="_blank" >RIV/67985904:_____/23:00576852 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11310/23:10474055

Výsledek na webu

<a href="https://www.embopress.org/doi/full/10.15252/embr.202256530" target="_blank" >https://www.embopress.org/doi/full/10.15252/embr.202256530</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.15252/embr.202256530" target="_blank" >10.15252/embr.202256530</a>

Jazyk výsledku

angličtina

Název v původním jazyce

CHK1-CDC25A-CDK1 regulate cell cycle progression and protect genome integrity in early mouse embryos

Popis výsledku v původním jazyce

After fertilization, remodeling of the oocyte and sperm genomes is essential to convert these highly differentiated and transcriptionally quiescent cells into early cleavage-stage blastomeres that are transcriptionally active and totipotent. This developmental transition is accompanied by cell cycle adaptation, such as lengthening or shortening of the gap phases G1 and G2. However, regulation of these cell cycle changes is poorly understood, especially in mammals. Checkpoint kinase 1 (CHK1) is a protein kinase that regulates cell cycle progression in somatic cells. Here, we show that CHK1 regulates cell cycle progression in early mouse embryos by restraining CDK1 kinase activity due to CDC25A phosphatase degradation. CHK1 kinase also ensures the long G2 phase needed for genome activation and reprogramming gene expression in two-cell stage mouse embryos. Finally, Chk1 depletion leads to DNA damage and chromosome segregation errors that result in aneuploidy and infertility.

Název v anglickém jazyce

CHK1-CDC25A-CDK1 regulate cell cycle progression and protect genome integrity in early mouse embryos

Popis výsledku anglicky

After fertilization, remodeling of the oocyte and sperm genomes is essential to convert these highly differentiated and transcriptionally quiescent cells into early cleavage-stage blastomeres that are transcriptionally active and totipotent. This developmental transition is accompanied by cell cycle adaptation, such as lengthening or shortening of the gap phases G1 and G2. However, regulation of these cell cycle changes is poorly understood, especially in mammals. Checkpoint kinase 1 (CHK1) is a protein kinase that regulates cell cycle progression in somatic cells. Here, we show that CHK1 regulates cell cycle progression in early mouse embryos by restraining CDK1 kinase activity due to CDC25A phosphatase degradation. CHK1 kinase also ensures the long G2 phase needed for genome activation and reprogramming gene expression in two-cell stage mouse embryos. Finally, Chk1 depletion leads to DNA damage and chromosome segregation errors that result in aneuploidy and infertility.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10605 - Developmental biology

Projekt

<a href="/cs/project/GA20-27742S" target="_blank" >GA20-27742S: Rozdíly v regulaci kontrolních bodů buněčného cyklu mezi zygotou a 2-buněčným embryem</a><br>

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2023

Kód důvěrnosti údajů

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

Název periodika

Embo Reports

ISSN

1469-221X

e-ISSN

1469-3178

Svazek periodika

24

Číslo periodika v rámci svazku

10

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

22

Strana od-do

e56530

Kód UT WoS článku

001119180600001

EID výsledku v databázi Scopus

2-s2.0-85170519683