title: Chromatin modifications during oogenesis in the mouse: removal of somatic subtypes of histone H1 from oocyte chromatin occurs post-natally through a post-transcriptional mechanism.
abstract: We examined the distribution of the somatic subtypes of histone H1 and the variant subtype, H1(0), and their encoding mRNAs during oogenesis and early embryogenesis in the mouse. As detected using immunocytochemistry, somatic H1 was present in the nuclei of oocytes of 18-day embryos. Following birth, however, somatic H1 became less abundant in both growing and non-growing oocytes, beginning as early as 4 days of age in the growing oocytes, and was scarcely detectable by 19 days. Together with previous results, this defines a period of time when somatic H1 is depleted in oocytes, namely, from shortly after birth when the oocytes are at prophase I until the 4-cell stage following fertilization. At the stages when somatic H1 was undetectable, oocyte nuclei could be stained using an antibody raised against histone H1(0), which suggests that this may be a major linker histone in these cells. In contrast to the post-natal loss of somatic H1 protein, mRNAs encoding four (H1a, H1b, H1d, H1e) of the five somatic subtypes were present, as detected using RT-PCR in growing oocytes of 9-day pups, and all five subtypes including H1c were present in fully grown oocytes of adults. All five subtypes were also present in embryos, both before and after activation of the embryonic genome. mRNA encoding H1(0) was also detected in oocytes and early embryos. Whole-mount in situ hybridization using cloned H1c and H1e cDNAs revealed that the mRNAs were present in the cytoplasm of oocytes and 1-cell embryos, in contrast to the sea urchin early embryo where they are sequestered in the cell nucleus. We suggest that, as in many somatic cell types, the chromatin of mouse oocytes becomes depleted of somatic H1 and relatively enriched in histone H1(0) postnatally, and that somatic H1 is reassembled onto chromatin in cleavage-stage embryos. The post-natal loss of somatic H1 appears to be regulated post-transcriptionally by a mechanism not involving nuclear localization.
authors.affiliation: Department of Obstetrics and Gynecology, Royal Victoria Hospital, Montreal, Quebec, Canada. hugh@rvhob2.lan.mcgill.ca
authors.forename: H J
authors.initials: HJ
authors.lastname: Clarke
authors.forename: M
authors.initials: M
authors.lastname: Bustin
authors.forename: C
authors.initials: C
authors.lastname: Oblin
mesh_terms: D000818:Animals; D001483:Base Sequence; D002467:Cell Nucleus / Q000378:metabolism; D002843:Chromatin / Q000378:metabolism*; D017931:DNA Primers; D004622:Embryo, Mammalian; D005260:Female; D019084:Fluorescent Antibody Technique, Indirect; D006657:Histones / Q000235:genetics / Q000378:metabolism*; D007124:Immunoenzyme Techniques; D051379:Mice; D008969:Molecular Sequence Data; D009865:Oocytes / Q000378:metabolism*; D009866:Oogenesis; D011247:Pregnancy; D012323:RNA Processing, Post-Transcriptional; D012333:RNA, Messenger
chemical_list: D002843:Chromatin; D017931:DNA Primers; D006657:Histones; D012333:RNA, Messenger