Greatwall-Endos-PP2A/B55 Twins network regulates translation and stability of maternal transcripts in the Drosophila oocyte-to-embryo transition

Author:

Rangone Hélène1ORCID,Bond Laura1,Weil Timothy T.2,Glover David M.13ORCID

Affiliation:

1. Department of Genetics, University of Cambridge, Downing Street , Cambridge, UK

2. Department of Zoology, University of Cambridge, Downing Street , Cambridge, UK

3. Division of Biology and Biological Engineering, California Institute of Technology, 1200 E. California Blvd , Pasadena, CA 91125, USA

Abstract

The transition from oocyte to embryo requires translation of maternally provided transcripts that in Drosophila is activated by Pan Gu kinase to release a rapid succession of 13 mitotic cycles. Mitotic entry is promoted by several protein kinases that include Greatwall/Mastl, whose Endosulfine substrates antagonize Protein Phosphatase 2A (PP2A), facilitating mitotic Cyclin-dependent kinase 1/Cyclin B kinase activity. Here we show that hyperactive greatwall Scant can not only be suppressed by mutants in its Endos substrate but also by mutants in Pan Gu kinase subunits. Conversely, mutants in me31B or trailer hitch, which encode a complex that represses hundreds of maternal mRNAs, enhance greatwall Scant . Me31B and Trailer Hitch proteins, known substrates of Pan Gu kinase, copurify with Endos. This echoes findings that budding yeast Dhh1, orthologue of Me31B, associates with Igo1/2, orthologues of Endos and substrates of the Rim15, orthologue of Greatwall. endos- derived mutant embryos show reduced Me31B and elevated transcripts for the mitotic activators Cyclin B, Polo and Twine/Cdc25. Together, our findings demonstrate a previously unappreciated conservation of the Greatwall–Endosulfine pathway in regulating translational repressors and its interactions with the Pan Gu kinase pathway to regulate translation and/or stability of maternal mRNAs upon egg activation.

Funder

NIH

Wellcome Trust

Publisher

The Royal Society

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