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DNA damage response during mouse oocyte maturation

A. Mayer, V. Baran, Y. Sakakibara, A. Brzakova, I. Ferencova, J. Motlik, TS. Kitajima, RM. Schultz, P. Solc,

. 2016 ; 15 (4) : 546-58. [pub] 20160108

Jazyk angličtina Země Spojené státy americké

Typ dokumentu časopisecké články, Research Support, N.I.H., Extramural, práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/bmc17000679
E-zdroje Online Plný text

NLK Free Medical Journals od 2002 do Před 1 rokem
PubMed Central od 2008 do Před 1 rokem
Europe PubMed Central od 2009 do Před 1 rokem

Odkazy

PubMed 26745237
DOI 10.1080/15384101.2015.1128592
Knihovny.cz E-zdroje

Because low levels of DNA double strand breaks (DSBs) appear not to activate the ATM-mediated prophase I checkpoint in full-grown oocytes, there may exist mechanisms to protect chromosome integrity during meiotic maturation. Using live imaging we demonstrate that low levels of DSBs induced by the radiomimetic drug Neocarzinostatin (NCS) increase the incidence of chromosome fragments and lagging chromosomes but do not lead to APC/C activation and anaphase onset delay. The number of DSBs, represented by γH2AX foci, significantly decreases between prophase I and metaphase II in both control and NCS-treated oocytes. Transient treatment with NCS increases >2-fold the number of DSBs in prophase I oocytes, but less than 30% of these oocytes enter anaphase with segregation errors. MRE11, but not ATM, is essential to detect DSBs in prophase I and is involved in H2AX phosphorylation during metaphase I. Inhibiting MRE11 by mirin during meiotic maturation results in anaphase bridges and also increases the number of γH2AX foci in metaphase II.  Compromised DNA integrity in mirin-treated oocytes indicates a role for MRE11 in chromosome integrity during meiotic maturation.

Citace poskytuje Crossref.org

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