High mobility group 1 protein (HMG1) has traditionally been considered a structural component of chromatin, possibly similar in function to histone H1. In fact, at the onset of Xenopus and Drosophila development, HMG1 appears to substitute for histone H1: HMG1 is abundant when histone H1 is absent after the midblastula transition histone H1 largely replaces HMG1. We show that in early mouse embryos the expression patterns of HMG1 and histone H1 are not complementary. Instead, HMG1 content increases after zygotic genome activation at the same time as histone H1. HMG1 does not remain associated to mitotic chromosomes either in embryos or somatic cells. These results argue against a shared structural role for HMG1 and histone H1 in mammalian chromatin.
In order to characterize the changes that occur in the population of maternally inherited transcripts before the transition from maternal to zygotic control of embryonic development (MZT) in mammals, we used rabbit embryos where zygotic transcription becomes necessary only after the fourth cleavage division, during the second day that follows fertilization. In the present work we have associated mRNA differential display and an RT-PCR based-method that allows amplification of the whole population of messengers to identify and characterize maternal transcripts which are degraded throughout this early period of development. While there is no major degradation of the polyA RNA population before MZT we identify 4 transcripts which progressively disappear up until the 8-16 cell stage. We also show that the degradation of one of these maternal messengers is controlled by zygotic transcription, which is not the case for the three others. This messenger shows homology with the human FGF9 gene and is potentially a good candidate to address the question of the molecular control of maternal to zygotic transition in early mammalian embryogenesis.
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