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Redistribution of nuclear antigens linked to cell proliferation and RNA processing in mouse oocytes and early embryos
Author(s) -
Vautier Dominique,
Besombes Didier,
Chassoux Danielle,
Aubry Florence,
Debey Pascale
Publication year - 1994
Publication title -
molecular reproduction and development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 105
eISSN - 1098-2795
pISSN - 1040-452X
DOI - 10.1002/mrd.1080380202
Subject(s) - biology , snrnp , microbiology and biotechnology , nuclear protein , cell nucleus , zygote , oocyte , embryo , blastomere , mitosis , interphase , antigen , embryogenesis , ribonucleoprotein , rna , genetics , cytoplasm , gene , transcription factor
Abstract We have systematically analyzed by indirect immunofluorescence the subcellular distribution of nuclear antigens in relation to developmental stages of maturing mouse oocytes and developing embryos. Antigens were of two types: (1) a protein whose nuclear localization in interphase somatic cells depends on their proliferative state protein recognized by a monoclonal antibody 43B1N, and (2) snRNP polypeptides recognized by autoimmune sera of anti‐Sm and anti‐RNP type. The protein recognized by 43B1N was present in the germinal vesicle of oocytes from antral follicles, but absent from the nuclei during the first hours of embryonic life up to the middle to late 2‐cell stage. Starting from this stage, it was always found in nuclei of interphase blastomeres, where its “speckles”; co‐localized with the speckles containing high concentrations of snRNP polypeptides. SnRNP polypeptides recognized by anti‐Sm and anti‐RNP sera were in turn found in nuclei of all developmental stages. When embryos were treated with aphidicolin or cytochalasin D to arrest cell division, the 43B1N reacting protein was again localized in the pronuclei at 42 hr post‐hCG, i.e., slightly later than the onset of transcriptional activity. These results suggest a progressive building up of nuclei during embryonic development, which could influence gene expression. © 1994 Wiley‐Liss, Inc.