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Literature DB >> 25694116

Stella preserves maternal chromosome integrity by inhibiting 5hmC-induced γH2AX accumulation.

Tsunetoshi Nakatani¹, Kazuo Yamagata², Tohru Kimura³, Masaaki Oda⁴, Hiroyuki Nakashima⁵, Mayuko Hori², Yoichi Sekita⁶, Tatsuhiko Arakawa⁵, Toshinobu Nakamura⁷, Toru Nakano⁸.

Abstract

In the mouse zygote, Stella/PGC7 protects 5-methylcytosine (5mC) of the maternal genome from Tet3-mediated oxidation to 5-hydroxymethylcytosine (5hmC). Although ablation of Stella causes early embryonic lethality, the underlying molecular mechanisms remain unknown. In this study, we report impaired DNA replication and abnormal chromosome segregation (ACS) of maternal chromosomes in Stella-null embryos. In addition, phosphorylation of H2AX (γH2AX), which has been reported to inhibit DNA replication, accumulates in the maternal chromatin of Stella-null zygotes in a Tet3-dependent manner. Cell culture assays verified that ectopic appearance of 5hmC induces abnormal accumulation of γH2AX and subsequent growth retardation. Thus, Stella protects maternal chromosomes from aberrant epigenetic modifications to ensure early embryogenesis.

Entities: Chemical Disease Gene Species

Keywords: 5‐hydroxymethylcytosine; Stella; Tet3; gammaH2AX; zygote

Mesh：

Substances：

Year: 2015 PMID： 25694116 PMCID： PMC4428038 DOI： 10.15252/embr.201439427

Source DB: PubMed Journal: EMBO Rep ISSN： 1469-221X Impact factor: 8.807

29 in total

1. Abnormal chromosome segregation at early cleavage is a major cause of the full-term developmental failure of mouse clones.

Authors: Eiji Mizutani; Kazuo Yamagata; Tetsuo Ono; Satoshi Akagi; Masaya Geshi; Teruhiko Wakayama
Journal: Dev Biol Date: 2012-01-14 Impact factor: 3.582

2. PGC7 binds histone H3K9me2 to protect against conversion of 5mC to 5hmC in early embryos.

Authors: Toshinobu Nakamura; Yu-Jung Liu; Hiroyuki Nakashima; Hiroki Umehara; Kimiko Inoue; Shogo Matoba; Makoto Tachibana; Atsuo Ogura; Yoichi Shinkai; Toru Nakano
Journal: Nature Date: 2012-06-03 Impact factor: 49.962

3. Selective killing of ATM- or p53-deficient cancer cells through inhibition of ATR.

Authors: Philip M Reaper; Matthew R Griffiths; Joanna M Long; Jean-Damien Charrier; Somhairle Maccormick; Peter A Charlton; Julian M C Golec; John R Pollard
Journal: Nat Chem Biol Date: 2011-04-13 Impact factor: 15.040

4. Cell cycle restriction by histone H2AX limits proliferation of adult neural stem cells.

Authors: Ruani N Fernando; Boris Eleuteri; Shaimaa Abdelhady; Andre Nussenzweig; Michael Andäng; Patrik Ernfors
Journal: Proc Natl Acad Sci U S A Date: 2011-03-21 Impact factor: 11.205

5. Replication-dependent loss of 5-hydroxymethylcytosine in mouse preimplantation embryos.

Authors: Azusa Inoue; Yi Zhang
Journal: Science Date: 2011-09-22 Impact factor: 47.728

6. High basal γH2AX levels sustain self-renewal of mouse embryonic and induced pluripotent stem cells.

Authors: Valentina Turinetto; Luca Orlando; Yolanda Sanchez-Ripoll; Benjamin Kumpfmueller; Michael P Storm; Paola Porcedda; Valentina Minieri; Silvia Saviozzi; Lisa Accomasso; Elisa Cibrario Rocchietti; Kim Moorwood; Paola Circosta; Alessandro Cignetti; Melanie J Welham; Claudia Giachino
Journal: Stem Cells Date: 2012-07 Impact factor: 6.277

7. Generation and replication-dependent dilution of 5fC and 5caC during mouse preimplantation development.

Authors: Azusa Inoue; Li Shen; Qing Dai; Chuan He; Yi Zhang
Journal: Cell Res Date: 2011-11-29 Impact factor: 25.617

8. Reprogramming of the paternal genome upon fertilization involves genome-wide oxidation of 5-methylcytosine.

Authors: Khursheed Iqbal; Seung-Gi Jin; Gerd P Pfeifer; Piroska E Szabó
Journal: Proc Natl Acad Sci U S A Date: 2011-02-14 Impact factor: 11.205

9. The role of Tet3 DNA dioxygenase in epigenetic reprogramming by oocytes.

Authors: Tian-Peng Gu; Fan Guo; Hui Yang; Hai-Ping Wu; Gui-Fang Xu; Wei Liu; Zhi-Guo Xie; Linyu Shi; Xinyi He; Seung-gi Jin; Khursheed Iqbal; Yujiang Geno Shi; Zixin Deng; Piroska E Szabó; Gerd P Pfeifer; Jinsong Li; Guo-Liang Xu
Journal: Nature Date: 2011-09-04 Impact factor: 49.962

10. Histone H2AX-dependent GABA(A) receptor regulation of stem cell proliferation.

Authors: Michael Andäng; Jens Hjerling-Leffler; Annalena Moliner; T Kalle Lundgren; Gonçalo Castelo-Branco; Evanthia Nanou; Ester Pozas; Vitezslav Bryja; Sophie Halliez; Hiroshi Nishimaru; Johannes Wilbertz; Ernest Arenas; Martin Koltzenburg; Patrick Charnay; Abdeljabbar El Manira; Carlos F Ibañez; Patrik Ernfors
Journal: Nature Date: 2008-01-09 Impact factor: 49.962

7 in total

Stella preserves maternal chromosome integrity by inhibiting 5hmC-induced γH2AX accumulation.

1. Abnormal chromosome segregation at early cleavage is a major cause of the full-term developmental failure of mouse clones.

2. PGC7 binds histone H3K9me2 to protect against conversion of 5mC to 5hmC in early embryos.

3. Selective killing of ATM- or p53-deficient cancer cells through inhibition of ATR.

4. Cell cycle restriction by histone H2AX limits proliferation of adult neural stem cells.

5. Replication-dependent loss of 5-hydroxymethylcytosine in mouse preimplantation embryos.

6. High basal γH2AX levels sustain self-renewal of mouse embryonic and induced pluripotent stem cells.

7. Generation and replication-dependent dilution of 5fC and 5caC during mouse preimplantation development.

8. Reprogramming of the paternal genome upon fertilization involves genome-wide oxidation of 5-methylcytosine.

9. The role of Tet3 DNA dioxygenase in epigenetic reprogramming by oocytes.

10. Histone H2AX-dependent GABA(A) receptor regulation of stem cell proliferation.

1. TET3-mediated DNA oxidation promotes ATR-dependent DNA damage response.

2. EHMT2 and SETDB1 protect the maternal pronucleus from 5mC oxidation.

Review 3. Alternative roles for oxidized mCs and TETs.

4. Embryonic defects induced by maternal obesity in mice derive from Stella insufficiency in oocytes.

5. SUV4-20 activity in the preimplantation mouse embryo controls timely replication.

6. Stella modulates transcriptional and endogenous retrovirus programs during maternal-to-zygotic transition.

7. Potential Roles of Intrinsic Disorder in Maternal-Effect Proteins Involved in the Maintenance of DNA Methylation.