333 research outputs found

    A Deepened Perspective: Under the Bridge

    Get PDF

    Epigenetic memory in plants.

    Get PDF
    Epigenetics refers to heritable changes in patterns of gene expression that occur without alterations in DNA sequence. The epigenetic mechanisms involve covalent modifications of DNA and histones, which affect transcriptional activity of chromatin. Since chromatin states can be propagated through mitotic and meiotic divisions, epigenetic mechanisms are thought to provide heritable 'cellular memory'. Here, we review selected examples of epigenetic memory in plants and briefly discuss underlying mechanisms.This work was supported by the Gatsby Charitable Foundation and the European Research Council.This is the author accepted manuscript. The final version is available from EMBO Press via http://dx.doi.org/10.15252/embj.20148888

    Epigenetic memory in plants

    Get PDF
    Epigenetics refers to heritable changes in patterns of gene expression that occur without alterations in DNA sequence. The epigenetic mechanisms involve covalent modifications of DNA and histones, which affect transcriptional activity of chromatin. Since chromatin states can be propagated through mitotic and meiotic divisions, epigenetic mechanisms are thought to provide heritable ‘cellular memory’. Here, we review selected examples of epigenetic memory in plants and briefly discuss underlying mechanisms.This work was supported by the Gatsby Charitable Foundation and the European Research Council.This is the author accepted manuscript. The final version is available from EMBO Press via http://dx.doi.org/10.15252/embj.20148888

    Untersuchung zur Erregungskopplung im glattmuskulären Magenantrum der Ratte mittels mehrdimensionaler korrelativer Netzwerkanalyse

    Get PDF
    Das Magenantrum der Ratte ist gekennzeichnet durch ein stark synchronisiertes phasisch-rhythmisches Kontraktionsverhalten, realisiert in einem multizellulären Netzwerk aus glatten Muskelzellen und interstitiellen Zellen nach Cajal, moduliert durch enterische und vegetative Nervenfasern. In der vorliegenden Arbeit wurde die interzelluläre glattmuskuläre Kopplung des spontan aktiven Gewebes mittels konfokaler Laser-Scanning-Mikroskopie und anschließender korrelativer Netzwerkanalyse charakterisiert und damit zur Klärung der Frage der Signalpropagation beigetragen

    Production of poly(GA) in C9ORF72 patient motor neurons derived from induced pluripotent stem cells

    Get PDF
    GGGGCC (G4C2) repeat expansion in the first intron of C9ORF72 is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). A key pathological hallmark of C9ORF72-related ALS/FTD is the accumulation of dipeptide repeat (DPR) proteins synthesized from both sense and antisense repeat RNAs in affected neurons.To investigate how DPR proteins are synthesized in C9ORF72 human neurons, we used CRISPR-Cas9 technology to generate a homozygous deletion in the first intron of C9ORF72, 5′ to the G4C2 repeats to assess the effect of this deletion on DPR production

    Lysinibacillus fusiformis M5 induces increased complexity in Bacillus subtilis 168 colony biofilms via hypoxanthine:Running Title: L. fusiformis M5 interaction with B. subtilis 168

    Get PDF
    ABSTRACT In recent years, biofilms have become a central subject of research in the fields of microbiology, medicine, agriculture, and systems biology, among others. The sociomicrobiology of multispecies biofilms, however, is still poorly understood. Here, we report a screening system that allowed us to identify soil bacteria which induce architectural changes in biofilm colonies when cocultured with Bacillus subtilis . We identified the soil bacterium Lysinibacillus fusiformis M5 as an inducer of wrinkle formation in B. subtilis colonies mediated by a diffusible signaling molecule. This compound was isolated by bioassay-guided chromatographic fractionation. The elicitor was identified to be the purine hypoxanthine using mass spectrometry and nuclear magnetic resonance (NMR) spectroscopy. We show that the induction of wrinkle formation by hypoxanthine is not dependent on signal recognition by the histidine kinases KinA, KinB, KinC, and KinD, which are generally involved in phosphorylation of the master regulator Spo0A. Likewise, we show that hypoxanthine signaling does not induce the expression of biofilm matrix-related operons epsABCDEFGHIJKLMNO and tasA-sipW-tapA . Finally, we demonstrate that the purine permease PbuO, but not PbuG, is necessary for hypoxanthine to induce an increase in wrinkle formation of B. subtilis biofilm colonies. Our results suggest that hypoxanthine-stimulated wrinkle development is not due to a direct induction of biofilm-related gene expression but rather is caused by the excess of hypoxanthine within B. subtilis cells, which may lead to cell stress and death. IMPORTANCE Biofilms are a bacterial lifestyle with high relevance regarding diverse human activities. Biofilms can be beneficial, for instance, in crop protection. In nature, biofilms are commonly found as multispecies communities displaying complex social behaviors and characteristics. The study of interspecies interactions will thus lead to a better understanding and use of biofilms as they occur outside laboratory conditions. Here, we present a screening method suitable for the identification of multispecies interactions and showcase L. fusiformis as a soil bacterium that is able to live alongside B. subtilis and modify the architecture of its biofilms. </jats:p

    CRISPR deletion of the C9ORF72 promoter in ALS/FTD patient motor neurons abolishes production of dipeptide repeat proteins and rescues neurodegeneration

    Get PDF
    GGGGCC (G4C2) repeat expansion in the first intron of C9ORF72 is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Brain tissues from affected individuals show characteristic nuclear RNA foci containing the expanded repeat RNAs, as well as neuronal inclusions containing dipeptide repeat (DPR) proteins [poly(GA), poly(GP), poly(GR), poly(PR), and poly(PA)] resulting from the translation of both sense and antisense repeat RNAs in all reading frames. Although reduced C9ORF72 protein function may contribute to disease, the more likely drivers of disease are mechanisms related to a gain of toxic function. Currently, intense efforts are being made to identify disease mechanisms amenable for the development of therapeutic strategies. One promising avenue would be to prevent the production of the expanded repeat RNAs, such as by antisense oligonucleotides. Here, we tested another potential therapeutic approach: CRISPR/Cas9-based targeting of the promoter region

    About the origin of the acrocentric part of non-acrocentric satellited chromosomes in humans

    Get PDF
    Here we characterized 11 healthy carriers of a non-acrocentric satellited chromosomes der(A)t(A;acro)(pter or qter;p1?1.2) to determine the frequency of chromosome 15p and 22p in such rearrangement

    An Arabidopsis jmjC domain protein protects transcribed genes from DNA methylation at CHG sites

    Get PDF
    Differential cytosine methylation of genes and transposons is important for maintaining integrity of plant genomes. In Arabidopsis, transposons are heavily methylated at both CG and non-CG sites, whereas the non-CG methylation is rarely found in active genes. Our previous genetic analysis suggested that a jmjC domain-containing protein IBM1 (increase in BONSAI methylation 1) prevents ectopic deposition of non-CG methylation, and this process is necessary for normal Arabidopsis development. Here, we directly determined the genomic targets of IBM1 through high-resolution genome-wide analysis of DNA methylation. The ibm1 mutation induced extensive hyper-methylation in thousands of genes. Transposons were unaffected. Notably, long transcribed genes were most severely affected. Methylation of genes is limited to CG sites in wild type, but CHG sites were also methylated in the ibm1 mutant. The ibm1-induced hyper-methylation did not depend on previously characterized components of the RNAi-based DNA methylation machinery. Our results suggest novel transcription-coupled mechanisms to direct genic methylation not only at CG but also at CHG sites. IBM1 prevents the CHG methylation in genes, but not in transposons
    corecore