Project description:Barley is an old crop with a complex history. To deeply study history of barley domestication, we pursue a haplotype-based approach to connect diversity and population structure in wild and domesticated barley. We sequenced the genomes of 628 genebank accessions and 23 archaeological specimens. Using these data, we infer the spatiotemporal origins of haplotypes and map the contributions of different wild barley populations either during the initial phase of domestication or through later gene flow. Domestication genes and ancient DNA sequences corroborate our genome-wide analysis in present-day samples.
Project description:We define the promotoreome sequence and epigenetic architecture in barley embryos to both put it into evolutionary perspective and to serve as a reference for agricultural and research biotechnology in cereals.
Project description:A major challenge in biology is to determine how evolutionarily novel characters originate, however, mechanistic explanations for the origin of novelties are almost completely unknown. The evolution of mammalianM-BM- pregnancy is an excellent system in which to study the origin of novelties because extant mammals preserve major stages in the transition from egg-laying to live-birth. To determine the molecular bases of this transition we characterized the pregnant/gravid uterine transcriptome from tetrapods, including species in the three major mammalian lineages, and used ancestral transcriptome reconstruction to trace the evolutionary history of uterine gene expression. We show that thousands of genes evolved endometrial expression during the origins of mammalian pregnancy, including numerous genes that mediate maternal-fetal communication and immunotolerance.Furthermore we show that thousands of regulatory elements active inM-BM- decidualized human endometrial stromal cellsM-BM- are derived from ancient mammalian transposable elements which provided binding sites for transcription factors that mediate decidualization and endometrial cell-type identity.M-BM- Our results indicate that one of the defining mammalian novelties evolved via domestication of ancient mammalian transposable elements into hormone-responsive regulatory elements throughout the genome. Examination of histone modification and DNAse hypersensitivity in decidualized dESC
Project description:Affymetrix 6.0 SNP data for haplotype comparison of patients from two different families sharing the same homozygous mutation in TFRC, to determine if the families were related to each other Peripheral blood was used for patients who had no history of hematopoietic stem cell transplant (HSCT). Fibroblasts cell lines were used as a source of DNA for the individual who received HSCT.
Project description:PRDM9, a histone methyltransferase, initiates meiotic recombination by binding DNA at recombination hotspots and directing the position of DNA double-strand breaks (DSB). The DSB repair mechanism suggests that hotspots should eventually self-destruct, yet genome-wide recombination levels remain constant, a conundrum known as the hotspot paradox. To test if PRDM9 drives this evolutionary erosion, we compared activity of the Prdm9Cst allele in two Mus musculus subspecies, M.m. castaneus, in which Prdm9Cst arose, and M.m. domesticus, into which Prdm9Cst was introduced. Comparing these two strains, we find that haplotype differences at hotspots leads to qualitative and quantitative changes in PRDM9 binding and activity. Most variants affecting PRDM9Cst binding arose and were fixed in M.m castaneus, suppressing hotspot activity. Furthermore, M.m castaneus x M.m domesticus F1 hybrids exhibit novel hotspots, representing sites of historic evolutionary erosion. Together these data support a model where haplotype-specific PRDM9 binding directs biased gene conversion at hotspots, ultimately leading to hotspot erosion. Identify position of meiotic H3K4me3 from various sub-species of mice and F1 hybrids from crosses between subspecies. In addition, perform ChIP-seq analysis on the meiosis-specific methyltransferase PRDM9.