No abstract

MEDEA (MEA) is an Arabidopsis Polycomb group gene that is imprinted in the endosperm. The maternal allele is expressed and the paternal allele is silent. MEA is controlled by DEMETER (DME), a DNA glycosylase required to activate MEA expression, and METHYLTRANSFERASE I (MET1), which maintains CG methylation at the MEA locus. Here we show that DME is responsible for endosperm maternal-allele-specific hypomethylation at the MEA gene. DME can excise 5-methylcytosine in vitro and when expressed in E. coli. Abasic sites opposite 5-methylcytosine inhibit DME activity and might prevent DME from generating double-stranded DNA breaks. Unexpectedly, paternal-allele silencing is not controlled by DNA methylation. Rather, Polycomb group proteins that are expressed from the maternal genome, including MEA, control paternal MEA silencing. Thus, DME establishes MEA imprinting by removing 5-methylcytosine to activate the maternal allele. MEA imprinting is subsequently maintained in the endosperm by maternal MEA silencing the paternal allele.

Cytosine DNA methylation is considered to be a stable epigenetic mark, but active demethylation has been observed in both plants and animals. In Arabidopsis thaliana, DNA glycosylases of the DEMETER (DME) family remove methylcytosines from DNA. Demethylation by DME is necessary for genomic imprinting, and demethylation by a related protein, REPRESSOR OF SILENCING1, prevents gene silencing in a transgenic background. However, the extent and function of demethylation by DEMETER-LIKE (DML) proteins in WT plants is not known. Using genome-tiling microarrays, we mapped DNA methylation in mutant and WT plants and identified 179 loci actively demethylated by DML enzymes. Mutations in DML genes lead to locus-specific DNA hypermethylation. Reintroducing WT DML genes restores most loci to the normal pattern of methylation, although at some loci, hypermethylated epialleles persist. Of loci demethylated by DML enzymes, >80% are near or overlap genes. Genic demethylation by DML enzymes primarily occurs at the 5 and 3 ends, a pattern opposite to the overall distribution of WT DNA methylation. Our results show that demethylation by DML DNA glycosylases edits the patterns of DNA methylation within the Arabidopsis genome to protect genes from potentially deleterious methylation. DNA glycosylase ͉ epigenetics ͉ genome maintenanceA rabidopsis is a eukaryotic model for DNA methylation studies. In Arabidopsis cytosine methylation is found in all sequence contexts (CG, CNG, and CNN) and is important for genomic imprinting and genome defense against transposable elements (1). Most DNA methylation is located at transposonrich heterochromatic regions (2-4). However, genome-wide mapping of methylation has showed that a significant fraction (20-33%) of genes are methylated (3-5). In general, methylation within Arabidopsis genes is concentrated in the middle and distributed away from 5Ј and 3Ј ends, suggesting that 5Ј and 3Ј methylation is detrimental to gene function (3, 4). The mechanisms that maintain gene ends relatively free of methylation are not known.DNA methylation is often considered a stable epigenetic mark, but enzymatic DNA demethylation is known to occur. In mammals, the paternal pronucleus is actively demethylated immediately after fertilization (6, 7) but the enzymes responsible are unknown (8). In Arabidopsis, DNA demethylation is mediated by the DEMETER (DME) family of bifunctional helixhairpin-helix DNA glycosylases that have both DNA glycosylase and apurinic/apyrimidinic (AP) lyase activities (9-13). The DNA glycosylase initiates the base excision repair process by specifically excising 5-methylcytosine through cleavage of the N-glycosylic bond. AP lyase subsequently nicks the DNA, and an AP endonuclease generates a 3Ј-hydroxyl to which a DNA repair polymerase adds an unmethylated cytosine. DNA ligase completes the repair process by sealing the nick.Demethylation by DME is one step in a developmental pathway that establishes genomic imprinting in the Arabidopsis endosperm (9,10,14). Three targets of DME are MEDEA (MEA),...

BackgroundTransposable elements are major evolutionary forces which can cause new genome structure and species diversification. The role of transposable elements in the expansion of nucleotide-binding and leucine-rich-repeat proteins (NLRs), the major disease-resistance gene families, has been unexplored in plants.ResultsWe report two high-quality de novo genomes (Capsicum baccatum and C. chinense) and an improved reference genome (C. annuum) for peppers. Dynamic genome rearrangements involving translocations among chromosomes 3, 5, and 9 were detected in comparison between C. baccatum and the two other peppers. The amplification of athila LTR-retrotransposons, members of the gypsy superfamily, led to genome expansion in C. baccatum. In-depth genome-wide comparison of genes and repeats unveiled that the copy numbers of NLRs were greatly increased by LTR-retrotransposon-mediated retroduplication. Moreover, retroduplicated NLRs are abundant across the angiosperms and, in most cases, are lineage-specific.ConclusionsOur study reveals that retroduplication has played key roles for the massive emergence of NLR genes including functional disease-resistance genes in pepper plants.Electronic supplementary materialThe online version of this article (doi:10.1186/s13059-017-1341-9) contains supplementary material, which is available to authorized users.

Susceptibility of chemical sensors to false positive signals remains a common drawback due to insufficient sensor coating selectivity. By mimicking biology, we have demonstrated the use of sequence-specific biopolymers to generate highly selective receptors for trinitrotoluene and 2,4-dinitrotoluene. Using mutational analysis, we show that the identified binding peptides recognize the target substrate through multivalent binding with key side chain amino acid elements. Additionally, our peptide-based receptors embedded in a hydrogel show selective binding to target molecules in the gas phase. These experiments demonstrate the technique of receptor screening in liquid to be translated to selective gas-phase target binding, potentially impacting the design of a new class of sensor coatings.

We extend the halo-independent method to compare direct dark matter detection data, so far used only for spin-independent WIMP-nucleon interactions, to any type of interaction. As an example we apply the method to magnetic moment interactions. †

Gene imprinting, the differential expression of maternal and paternal alleles, independently evolved in mammals and in flowering plants. A unique feature of flowering plants is a double-fertilization event in which the sperm fertilize not only the egg, which forms the embryo, but also the central cell, which develops into the endosperm (an embryo-supporting tissue). The distinctive mechanisms of gene imprinting in the endosperm, which involve DNA demethylation and histone methylation, begin in the central cell and sperm prior to fertilization. Flowering plants might have coevolved double fertilization and imprinting to prevent parthenogenetic development of the endosperm.

We present comparisons of direct detection data for "light WIMPs" with an anapole moment interaction (ADM) and a magnetic dipole moment interaction (MDM), both assuming the Standard Halo Model (SHM) for the dark halo of our galaxy and in a halo-independent manner. In the SHM analysis we find that a combination of the 90% CL LUX and CDMSlite limits or the new 90% CL SuperCDMS limit by itself exclude the parameter space regions allowed by DAMA, CoGeNT and CDMS-II-Si data for both ADM and MDM. In our halo-independent analysis the new LUX bound excludes the same potential signal regions as the previous XENON100 bound. Much of the remaining signal regions is now excluded by SuperCDMS, while the CDMSlite limit is much above them. The situation is of strong tension between the positive and negative search results both for ADM and MDM. We also clarify the confusion in the literature about the ADM scattering cross section.