In mammals, fusion of two morphologically distinct gametes, oocytes and spermatozoa, leads to the formation of totipotent embryos. Acquisition of totipotency is thought to be mediated by extensive epigenetic reprogramming of parental genomes, affecting DNA methylation and histone modifications, and possibly replication timing and transcriptional activity in parental specific manners [1][2][3][4] . It is currently unclear to what extent differential reprogramming of maternal and paternal genomes is due to differences in chromatin states inherited from the oocyte and spermatozoon [4][5][6][7][8][9][10][11] . Beyond DNA methylation 1,2,6,12 , it is unknown which types of parental chromatin states are maintained or reprogrammed in early embryos. If certain parental chromatin states did escape reprogramming in the early embryo, such information could constitute an "intrinsic intergenerational epigenetic program directing gene expression in the next generation 13 . If these chromatin states also escaped reprogramming during gametogenesis, the inheritance program would function transgenerationally 13 . An increasing number of studies point to inter-or transgenerational transmission of acquired phenotypic traits that are related to temporal exposure of (grand-)parents to alternative instructive environmental cues [14][15][16][17][18] . Mechanistically, such phenotypic changes may be related to (transient) alterations of an intrinsic inheritance program.A role of histones and associated posttranslational modifications in maternal and paternal transmission of intrinsic or acquired epigenetic information is largely unknown 13 . In many metazoans, male germ cells undergo during their final differentiation into sperm an extensive chromatin remodeling process during which 3 genomic DNA becomes newly packaged into a highly condensed configuration by sperm specific proteins. In mammals, removal of histones is generally not complete 10,11,[19][20][21][22][23][24] . Furthermore, remaining histones have been reported to stay associated with the paternal genome during de novo chromatin formation in the zygote following fertilization 9 .We and others recently showed that histones lasting in human sperm are to some extent enriched at regulatory sequences of genes 10,11 . We also demonstrated that H3K4me3-and H3K27me3-marked histones are retained at promoters of specific sets of genes in mouse spermatozoa 11. The extent of evolutionary conservation of nucleosome retention at gene regulatory sequences in spermatozoa and the mechanistic principles of such retention are, however, unknown.To address conservation and to dissect the molecular logic underlying nucleosome retention, we determined the genome-wide nucleosome occupancy in mouse spermatozoa that only contain 1% residual histones. We show here that combinatorial effects of sequence composition, histone variants and histone modifications uniquely determine the packaging of sperm DNA. Nucleosomes in sperm mainly localize to unmethylated CpG-rich sequences in a histone variant specif...
Gene expression programs define shared and species-specific phenotypes, but their evolution remains largely uncharacterized beyond the transcriptome layer 1 . Here we report an analysis of the co-evolution of translatomes and transcriptomes using ribosome-profling and matched RNA-sequencing data for three organs (brain, liver and testis) in fve mammals (human, macaque, mouse, opossum and platypus) and a bird (chicken). Our within-species analyses reveal that translational regulation is widespread in the diferent organs, in particular across the spermatogenic cell types of the testis. The between-species divergence in gene expression is around 20% lower at the translatome layer than at the transcriptome layer owing to extensive buffering between the expression layers, which especially preserved old, essential and housekeeping genes. Translational upregulation specifcally counterbalanced global dosage reductions during the evolution of sex chromosomes and the efects of meiotic sex-chromosome inactivation during spermatogenesis. Despite the overall prevalence of bufering, some genes evolved faster at the translatome layer—potentially indicating adaptive changes in expression; testis tissue shows the highest fraction of such genes. Further analyses incorporating mass spectrometry proteomics data establish that the co-evolution of transcriptomes and translatomes is refected at the proteome layer. Together, our work uncovers co-evolutionary patterns and associated selective forces across the expression layers, and provides a resource for understanding their interplay in mammalian organs.
Retinoic acid (RA) is an essential extrinsic inducer of meiotic initiation in mammalian germ cells. However, RA acts too widely in mammalian development to account, by itself, for the cell-type and temporal specificity of meiotic initiation. We considered parallels to yeast, in which extrinsic and intrinsic factors combine to restrict meiotic initiation. We demonstrate that, in mouse embryos, extrinsic and intrinsic factors together regulate meiotic initiation. The mouse RNA-binding protein DAZL, which is expressed by postmigratory germ cells, is a key intrinsic factor, enabling those cells to initiate meiosis in response to RA. Within a brief developmental window, Dazl-expressing germ cells in both XX and XY embryos actively acquire the ability to interpret RA as a meiosis-inducing signal.
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