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19.06.18 RNA-binding protein SRSF3 shown to regulate the maternal transcriptome in mouse oocyte

last modified Jul 03, 2018 04:14 PM
The Surani lab, with colleagues in Cambridge, Norwich, London and Singapore, highlight the role of RNA-binding proteins in controlling the maternal transcriptome for correct development of fertilised oocytes
19.06.18 RNA-binding protein SRSF3 shown to regulate the maternal transcriptome in mouse oocyte

Fig 1a (extract): Immunostaining shows SRSF3 protein expression in preimplantation embryos

SRSF3 maintains transcriptome integrity in oocytes by regulation of alternative splicing and transposable elements

Vinh Do, D et al. (2018) Cell Discovery 4: 33. doi: 10.1038/s41421-018-0032-3


Abstract from the paper

The RNA-binding protein SRSF3 (also known as SRp20) has critical roles in the regulation of pre-mRNA splicing. Zygotic knockout of Srsf3 results in embryo arrest at the blastocyst stage. However, SRSF3 is also present in oocytes, suggesting that it might be critical as a maternally inherited factor. Here we identify SRSF3 as an essential regulator of alternative splicing and of transposable elements to maintain transcriptome integrity in mouse oocyte. Using 3D time-lapse confocal live imaging, we show that conditional deletion of Srsf3 in fully grown germinal vesicle oocytes substantially compromises the capacity of germinal vesicle breakdown (GVBD), and consequently entry into meiosis. By combining single cell RNA-seq, and oocyte micromanipulation with steric blocking antisense oligonucleotides and RNAse-H inducing gapmers, we found that the GVBD defect in mutant oocytes is due to both aberrant alternative splicing and derepression of B2 SINE transposable elements. Together, our study highlights how control of transcriptional identity of the maternal transcriptome by the RNA-binding protein SRSF3 is essential to the development of fertilized-competent oocytes.



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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