The p100 EBNA-2 coactivator: a highly conserved protein found in a range of exocrine and endocrine cells and tissues in cattle Broadhurst MK, et al .
The p100 transcriptional coactivator is an evolutionarily conserved protein that has been shown to be a coactivator of the Epstein-Barr virus-encoded transcription factor EBNA-2, as well as Stat5 and Stat6. However, the p100 genomic organisation, phylogeny and expression have not been analysed in detail and its physiological role is uncertain. The cDNA and amino acid sequence of bovine p100 was obtained, and the genomic organisation of the human p100 gene was determined. Homologues of p100 were found in the genomes of 21 diverse eukaryotes. Western blot and immunohistochemical analyses revealed that the bovine p100 protein is present in a range of exocrine and endocrine cells and tissues, including the lactating mammary gland, pancreas, adrenal, parotid, anterior pituitary, corpus luteum, ovarian follicular cells, placenta and small intestine. P100 was present in the nuclei of mammary epithelial cells and pancreatic acinar cells, but only in the extranuclear compartment of the other immunopositive tissues. These data indicate that the p100 protein plays a fundamental role in eukaryotic biology, and functions in secretory cells, at least in cattle.
General function
Nucleic acid binding, DNA binding, Transcription factor
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Cellular localization
Nuclear
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Ovarian function
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Expression regulated by
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Ovarian localization
Oocyte, Granulosa, Luteal cells
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Reprogramming of microRNAs by adenosine-to-inosine editing and the selective elimination of edited microRNA precursors in mouse oocytes and preimplantation embryos. Garca-Lpez J et al. Adenosine deaminases-acting-on-RNA (ADAR) proteins induce adenosine-to-inosine editing in double-stranded RNA molecules. This editing generates RNA diversity at the post-transcriptional level, and it has been implicated in the control of cell differentiation and development. The editing of microRNA (miRNA) precursors, along with Tudor-SN (Snd1) activity, could lead to the elimination of selected miRNAs and reprogram miRNA activity. Here, we report the dynamics of adenosine-to-inosine editing in miRNA precursors and their selected elimination during mouse preimplantation development. Adar1p110 and Snd1 were found to be strongly but differentially expressed in oocytes and zygotes with respect to later pre-implantation stages. When the biogenesis of miR-151 was assessed, the majority of miR-151 precursors was edited and subsequently eliminated during early development. Deep sequencing of this and other miRNAs confirmed that, in general, edited precursors were selectively eliminated at early post-zygotic stages. Moreover, in oocytes and throughout the zygote-to-blastocyst stages, Tudor-SN accumulated in newly discovered aggregates termed 'T bodies'. These results provide new insight into how editing and Tudor-SN-mediated elimination of miRNA precursors is regulated during early development.