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10.05.18 Surani lab show epigenetic modifier G9a is vital in preimplanation embryo development

last modified Jun 11, 2018 10:19 AM
In this eLife paper the Surani lab examine effects of loss of maternally inherited G9a on regulation of cell fate choices at onset of embryo development
10.05.18 Surani lab show epigenetic modifier G9a is vital in preimplanation embryo development

Fig 2c (extract): E4.5 embryo with G9a maternal depletion shows aberrant lineage segregation.

G9a regulates temporal preimplantation developmental program and lineage segregation in blastocyst

Zylicz JJ et al. (2018) Elife 7:e33361 DOI: 10.7554/eLife.33361

 

 

Abstract from the paper

Early mouse development is regulated and accompanied by dynamic changes in chromatin modifications, including G9a-mediated histone H3 lysine 9 dimethylation (H3K9me2). Previously, we provided insights into its role in post-implantation development (Zylicz et al., 2015).

Here we explore the impact of depleting the maternally inherited G9a in oocytes on development shortly after fertilisation. We show that G9a accumulates typically at 4 to 8-cell stage to promote timely repression of a subset of 4-cell stage-specific genes. Loss of maternal inheritance of G9a disrupts the gene regulatory network resulting in developmental delay and destabilisation of inner cell mass lineages by the late blastocyst stage.

Our results indicate a vital role of this maternally inherited epigenetic regulator in creating conducive conditions for developmental progression and on cell fate choices.

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Read more about research in the Surani lab.

Studying development to understand disease

The Gurdon Institute is funded by Wellcome and Cancer Research UK to study the biology of development, and how normal growth and maintenance go wrong in cancer and other diseases.

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G9a regulates temporal preimplantation developmental program and lineage segregation in blastocyst

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