Élaboration et évaluation d'un matériel didactique relatif à l'apprentissage de la notion de fraction en cinquième année du primaire

Cette étude porte sur les difficultés reliées à l'apprentissage de la notion de fraction. Le but est d'élaborer et d'évaluer un document permettant de faciliter l'apprentissage de cette notion. La théorie de Piaget concernant l'acquisition des connaissances a été retenue comme élément de base dans la construction du matériel. Ainsi, chaque objectif étudié a été présenté en respectant une succession de trois étapes (concret, semi-concret, abstrait). La revue des écrits met en évidence les difficultés reliées a la qualité des documents utilisés auprès des enfants. Le matériel a été évalué selon l'approche L.V.R. (Learner Verification and Revision) afin d'augmenter son efficacité en vue de l'atteinte des objectifs. Cette étude vise à vérifier trois hypothèses. La première tente de déterminer si un matériel élaboré en respectant les étapes du processus d'apprentissage et soumis à une évaluation de type L.V.R. permet aux enfants de faire l'apprentissage de la notion de fraction. La seconde vérifie si les résultats obtenus par les enfants ayant utilisé ce matériel sont supérieurs (p<O,O5) à ceux des autres enfants. Finalement, la troisième hypothèse s'intéresse à la rétention en analysant les performances des enfants du groupe contrôle et du groupe expérimental quatre mois après l'expérimentation. c'est dans un cadre quasi expérimental que les résultats ont été recueillis. Ils démontrent que le matériel élaboré en tenant compte des étapes du processus d'apprentissage et soumis à une évaluation de type L.V.R. permet aux enfants de faire l'apprentissage de la notion de fraction. Ainsi ils obtiennent des performances moyennes de 80% aux fiches d'apprentissage. Leurs performances sont meilleures que celles des autres enfants quand on évalue à l'aide du test couvrant l'ensemble des objectifs présentés. De plus, l'écart entre les enfants du groupe contrôle et ceux du groupe expérimental se maintient, et même augmente, lorsqu'on évalue leurs performances quatre mois après l'expérimentation. On peut conclure que le respect des étapes du processus d'apprentissage et la qualité des documents utilisés facilitent l'apprentissage de la notion de fraction. Finalement, l'ensemble des informations recueillies conduisent a l'interrogation suivante: l'enseignement vise-t-il des performances immédiates ou la compréhension des notions

Conserved imprinting associated with unique epigenetic signatures in the Arabidopsis genus

In plants, imprinted gene expression occurs in endosperm seed tissue and is sometimes associated with differential DNA methylation between maternal and paternal alleles1. Imprinting is theorized to have been selected for because of conflict between parental genomes in offspring2, but most studies of imprinting have been conducted in Arabidopsis thaliana, an inbred primarily self-fertilizing species that should have limited parental conflict. We examined embryo and endosperm allele-specific expression and DNA methylation genome-wide in the wild outcrossing species Arabidopsis lyrata. Here we show that the majority of A. lyrata imprinted genes also exhibit parentally biased expression in A. thaliana, suggesting that there is evolutionary conservation in gene imprinting. Surprisingly, we discovered substantial interspecies differences in methylation features associated with paternally expressed imprinted genes (PEGs). Unlike in A. thaliana, the maternal allele of many A. lyrata PEGs was hypermethylated in the CHG context. Increased maternal allele CHG methylation was associated with increased expression bias in favour of the paternal allele. We propose that CHG methylation maintains or reinforces repression of maternal alleles of PEGs. These data suggest that the genes subject to imprinting are largely conserved, but there is flexibility in the epigenetic mechanisms employed between closely related species to maintain monoallelic expression. This supports the idea that imprinting of specific genes is a functional phenomenon, and not simply a byproduct of seed epigenomic reprogramming. Genomic imprinting is a form of epigenetic gene regulation in flowering plants and mammals in which alleles of genes are expressed in a parent-of-origin dependent manner. Allele-specific gene expression profiling has identified hundreds of imprinted genes in A. thaliana, maize and rice endosperm, the functions of which are largely unknown. Allelic differences in DNA methylation and chromatin modification between maternal and paternal alleles are important for establishing and maintaining imprinted expression. The emerging picture from multiple species is that the paternal allele of PEGs is associated with DNA methylation, and the silent maternal allele is hypomethylated and bears the Polycomb Repressive Complex 2 (PRC2) mark H3K27me3. Several evolutionary theories have been proposed to describe processes that would select for fixation of this unusual pattern of gene expression13. The kinship or parental conflict theory posits that imprinting is selected for because of asymmetric relatedness among kin. In species where the maternal parent directly provisions growing progeny and has offspring by multiple males, maternally and paternally inherited genomes are predicted to have conflicting interests with regard to the extent of maternal investment. Paternally inherited alleles are expected to favour maternal investment at the expense of half-siblings. Low conservation of imprinting between A. thaliana and monocots, limited conservation between rice and maize, evidence for intraspecific variation in imprinting and lack of strong phenotypes for some imprinted gene mutants has cast doubt on whether imprinting of particular genes is functionally important. Additionally, although some imprinted genes are associated with differential methylation, it has been suggested that imprinted expression is simply a byproduct of endosperm DNA methylation changes—changes that could have a primary function outside imprinting regulation. We were motivated by these considerations and by predictions of the parental conflict theory to compare imprinting and seed DNA methylation between two closely related species that differ in breeding strategy. A. lyrata and A. thaliana diverged approximately 13 Myr ago. Although A. thaliana outcrosses to some extent in the wild, as an obligate outcrosser A. lyrata should be subject to a higher degree of parental conflict than A. thaliana and should therefore be under greater pressure to maintain imprinting. To identify A. lyrata imprinted genes, we performed mRNA-seq on parental strains and F1 hybrid embryo and endosperm tissue derived from crosses between the sequenced A. lyrata strain MN47 (MN) and a strain from Karhumäki (Kar) (Supplementary Fig. 1, Supplementary Fig. 2 and Supplementary Tables 1 and 2). After reannotating A. lyrata genes based on our extensive RNA-seq data (see Supplementary Methods), sequence polymorphisms between MN and Kar were used to quantify the contributions of each parental genome to gene expression. All possible pairwise comparisons (n = 12) of parent-of-origin bias among three MN × Kar and four Kar × MN reciprocal cross-replicates were performed to identify imprinted genes using the same criteria we previously applied to A. thaliana. Only genes that were defined as imprinted in at least 40% of comparisons were included in the final set (Fig. 1 and Supplementary Tables 3 and 4, see Supplementary Methods for details of imprinting criteria). This analysis yielded 49 PEGs and 35 maternally expressed imprinted genes (MEGs) in endosperm (Fig. 1a). Allele assignment calls for 13 genes, including both imprinted and non-imprinted genes, were validated by pyrosequencing (Supplementary Fig. 3). As expected3,5, there was little evidence for imprinting in embryos (Fig. 1a). We compared A. lyrata and A. thaliana endosperm imprinted genes (Fig. 1, Supplementary Fig. 4 and Supplementary Table 4). Of the A. lyrata PEGs for which there were sufficient data available in A. thaliana, 72% (26/36) were also paternally biased in A. thaliana, with 50% (18/36) meeting all stringent criteria for being designated as a PEG in both species (Fig. 1b). Conserved PEGs encoded DNA binding proteins and genes related to chromatin modification, among others (Supplementary Table 4). Of the A. lyrata MEGs for which there were sufficient data in A. thaliana, 70% (12/17) were also significantly maternally biased in A. thaliana, with 35% (6/17) meeting all criteria for being called a MEG in both datasets (Fig. 1b). The conserved MEGs included the Polycomb group gene FIS2, the F-box gene SDC, another F-box gene and three genes encoding DNA binding proteins. Although previous research has identified somewhat more imprinted genes in A. thaliana than what we describe in A. lyrata, these studies involved multiple accessions and assessed imprinting for a greater total number of genes. The majority of genes that were imprinted in A. thaliana but not in A. lyrata lacked sufficient data to make an imprinting designation in A. lyrata (Supplementary Fig. 4). Thus, it is presently unclear whether the number of imprinted genes differs significantly between the species. All of the genes that are commonly imprinted among A. thaliana and cereals were also imprinted in A. lyrata. Many mammalian imprinted genes are clearly involved in growth regulation, including genes for nutrient uptake and feeding behaviour. By contrast, we found that proteins encoded by conserved plant imprinted genes were predicted to regulate or affect the expression of many other genes (chromatin proteins and transcription factors) or protein abundance (F-boxes). We also found that some pathways, rather than orthologous genes, were imprinted in both species, as has been previously noted for imprinting of different subunits of the PRC2 complex among Arabidopsis and cereals. In A. thaliana, the large subunit of RNA Polymerase IV, NRPD1, which functions in RNA-directed DNA methylation (RdDM), is a PEG5,6. Although we did not find evidence for imprinting of the NRPD1 gene in A. lyrata, homologues of two other genes involved in RdDM were PEGs (Supplementary Table 4): NRPD4/NRPE4/RDM2 (AL946699), which encodes a common subunit of Pol IV and Pol V, and RRP6L1 (AL337734), which encodes an exosomal protein that impacts RdDM. Thus, in both species the function of RdDM in the endosperm is under paternal influence, but this is achieved through different genes. The kinship theory is essentially an argument about optimal total gene expression levels in offspring. We therefore evaluated the expression levels and patterns of imprinted genes. MEGs appear to be primarily endosperm-specific genes; they have much lower than average expression in embryos and flower buds, and much higher than average expression in the endosperm (Fig. 1c). Conversely, PEGs were more highly expressed in all tissues than genes on average, and showed more modest expression increases in endosperm, suggesting that the expression of MEGs and PEGs is regulated differently. We also compared the percentage of maternal transcripts for homologous imprinted A. lyrata and A. thaliana genes (Fig. 1d). Conserved MEGs and PEGs exhibited similar degrees of parental bias in the two species (Fig. 1d). However, comparison of the A. thaliana and A. lyrata gene expression level for individual imprinted genes indicated that the overall expression level of PEGs was higher in A. lyrata than in A. thaliana (Fig. 1e). These findings are consistent with selection for higher expression of PEGs in species with greater parental conflict, such as obligate outcrossers. In A. thaliana, active DNA demethylation by the 5-methylcytosine DNA glycosylase DME in the central cell (the female gamete that is the progenitor of the endosperm) before fertilization is essential for establishing gene imprinting at many loci1. Imprinting of many A. thaliana genes, particularly PEGs, is correlated with maternal allele demethylation of proximal sequences corresponding to fragments of transposable elements (TEs). A. lyrata PEGs were somewhat enriched for the presence of TEs in 5′ regions compared with all genes, with 30 out of 49 PEGs (61%) associated with at least one TE within 2 kb upstream, compared with 51% of all genes (Supplementary Table 4). To test if the relationship between methylation and imprinting was conserved in A. lyrata, we profiled genome-wide methylation in MN × MN flower bud, embryo and endosperm tissue by whole-genome bisulfite sequencing. Shared and novel endosperm methylation features were observed compared with A. thaliana (Figs 2 and 3, Supplementary Fig. 5 and Supplementary Table 5). In plants, DNA methylation is found in CG, CHG and CHH sequence contexts. CG methylation was strongly decreased in TEs and in the 5′ and 3′ regions of genes in endosperm relative to other tissues (Fig. 2a and Supplementary Fig. 5). By profiling allele-specific DNA methylation in the F1 embryo and endosperm from Kar females crossed with MN males, we determined that maternally inherited DNA was primarily responsible for endosperm CG hypomethylation (Fig. 2b). These data suggest that, as in A. thaliana, A. lyrata maternally inherited genomes are actively demethylated before fertilization.By contrast, we were surprised to discover that A. lyrata endosperm had a non-CG DNA methylation profile distinct from A. thaliana. This was unexpected because DNA methylation patterns in A. lyrata vegetative tissues display similar features to A. thaliana, although overall methylation levels are higher (Supplementary Fig. 5). We found that average CHG methylation in gene bodies was increased in endosperm compared with embryo (Fig. 2a), a phenotype not observed in wild-type A. thaliana endosperm profiled at similar developmental stages (Supplementary Fig. 5). To determine whether differences in aggregate methylation profiles represented small changes in many regions or larger changes in specific regions of the genome, we compared embryo and endosperm methylation profiles to identify differentially methylated regions (DMRs). As in A. thaliana, the most abundant class of DMRs were less CG methylated in the endosperm than the embryo, with 38% of these falling within 2 kb upstream of genes and 34% within 2 kb downstream of genes (Supplementary Table 6). Regions that gained CHG methylation in MN × MN endosperm displayed markedly different characteristics; 84% fell within gene bodies, corresponding to 1,606 genes (Fig. 2c and Supplementary Table 6). CHG endosperm hypermethylated DMRs were also longer than all other DMR types (mean length = 564 bp with 400 bp s.d.) (Supplementary Table 6). CHG gene body hypermethylation was also observed in Kar × MN endosperm, although on fewer genes (n = 194). Allele-specific analysis of methylation indicated that endosperm CHG hypermethylation was specific to maternally inherited alleles (Fig. 2d). Methylation within gene bodies is usually restricted to the CG context, which is maintained after DNA replication by the maintenance methyltransferase MET1. CHG methylation, normally not found in genes, is maintained by the DNA methyltransferase CMT3, which directly binds to the repressive histone modification H3K9me2 (ref. 23). When accompanied by H3K9me2, CHG gene body methylation is associated with transcriptional repression24. We found that gain of gene body CHG methylation in A. lyrata endosperm was associated with reduced gene expression (Supplementary Fig. 6). Of the CHG hypermethylated genes with enough coverage to evaluate differential expression (n = 1,225), 338 were significantly less expressed in endosperm than in embryo, compared with 159 significantly more highly expressed in endosperm. This represents a significant enrichment of CHG hypermethylated genes among genes less expressed in endosperm than embryo (P = 1.766 × 10–21, hypergeometric test) and a significant depletion among genes upregulated in endosperm (P = 2.04 × 10–10, see Supplementary Methods). The mechanism responsible for CHG gene body hypermethylation in A. lyrata endosperm remains unclear. We found significant overlap between A. thaliana genes that gain CHG methylation or H3K9me2 in ibm1 mutants and CHG hypermethylation of orthologous genes in A. lyrata endosperm (Supplementary Fig. 7). IBM1 encodes a histone lysine demethylase that prevents accumulation of H3K9me2, and thus accumulation of CHG methylation, in genes24. IBM1 transcript abundance was lower in the endosperm than embryo (Supplementary Fig. 7). In A. thaliana, methylation in the long intron of IBM1 is required for proper transcript splicing and production of an enzymatically active protein25. We found that A. lyrata IBM1 exhibited decreased CG and non-CG methylation and increased accumulation of RNA-seq reads in the long intron in endosperm relative to embryo (Supplementary Fig. 7). However, A. thaliana endosperm also had reduced methylation in the long intron and decreased IBM1 transcript abundance than the embryo (Supplementary Fig. 7). Thus, differences in IBM1 expression alone are not sufficient to explain CHG hypermethylation in A. lyrata endosperm compared with A. thaliana, although reduced IBM1 activity is likely to be part of the mechanism. Several of the observed endosperm methylation features were correlated with gene imprinting. More than half of the A. lyrata MEGs and approximately one-third of PEGs were associated with endosperm CG hypomethylated DMRs in the 2 kb region upstream of the transcriptional start site, whereas only 11% of non-imprinted genes were similarly associated with these DMRs (Fig. 3, Supplementary Table 4, Supplementary Fig. 8 and Supplementary Fig. 9). CG hypomethylation occurred specifically on the maternally inherited allele (Supplementary Fig. 8). Thus, reduction of CG methylation by active demethylation is also likely to be an important component of the A. lyrata imprinting mechanism. We found a striking and non-mutually exclusive association between PEGs and endosperm CHG hypermethylation. Almost 60% of PEG gene bodies (n = 27) were CHG hypermethylated, and about one-third were also associated with a 5′ or 3′ CG hypomethylated DMR (Supplementary Table 4). The average methylation profile of PEGs containing a CHG endosperm hypermethylated DMR indicated a very strong increase in CHG methylation across the entire gene body, which was specific to the maternally inherited allele (Figs 3 and 4). Results were validated for two PEGs, homologues of AT5G10950 and AT5G26210, by locus-specific bisulfite-PCR (Fig. 4 and Supplementary Fig. 10). In both A. thaliana and A. lyrata these genes were associated with CG or CHH endosperm hypomethylated DMRs in 5′ To determine if there was a quantitative relationship between gain of CHG methylation and allelic expression bias, we plotted the difference in CHG methylation between maternal alleles in the embryo and endosperm relative to the ratio of maternal to paternal allele transcripts (Fig. 3c). The degree to which CHG methylation was gained on the maternal allele in endosperm relative to embryo was positively correlated with the extent of paternal allele expression bias in endosperm. In addition, PEGs were clearly distinct from other genes that gained CHG gene body methylation; they tended to exhibit greater gain of CHG methylation (Fig. 3c) and were also hypermethylated along more of their length than all CHG hypermethylated genes (56 versus 29%) (Supplementary Tables 4 and 6). Thus, a greater extent and amount of maternal allele CHG hypermethylation is correlated with more paternally biased transcription. These data suggest that CHG methylation, perhaps accompanied by gain of H3K9me2, represses the maternal alleles of PEGs. It is unknown whether gene body CHG methylation is established on maternal alleles before or after fertilization. Demethylation of the IBM1 regulatory intron (Supplementary Fig. 7) could be initiated before fertilization in the central cell, leading to its downregulation and an increase in CHG methylation specifically on maternal alleles, which would then be maintained after fertilization. Alternatively, if maternal allele CHG methylation occurs after fertilization, then CMT3 must be able to distinguish maternally and paternally inherited alleles. Retention of CG gene body methylation on the paternal alleles of PEGs (Fig. 4) could possibly protect them from gain of CHG methylation. Interestingly, gain of gene body CHG methylation was also recently shown to occur in both A. thaliana endosperm and embryos when wild-type plants were pollinated by diploid hypomethylated pollen. Diploid pollen creates triploid seeds with tetraploid endosperm that usually abort, but seed abortion is suppressed when the pollen is hypomethylated owing to mutations in met. Many of the genes that gain CHG methylation and have reduced expression in triploid rescued seeds are PEGs. However, this phenotype appears to be distinct from what we observed; the CHG methylation gain is much more modest than what we have described in wild-type A. lyrata endosperm, and only one conserved PEG was affected. Our data further suggest that gene body CHG hypermethylation is not a state restricted to mutant tissues, but can occur in a developmentally regulated manner that could be important for maintaining gene expression programmes. This is the first study to compare imprinting between two closely related plant species that differ in breeding strategy. A. lyrata and A. thaliana homologous imprinted genes are epigenetically modified in a distinct manner despite the close relatedness of the species (Fig. 4). Allele-specific maintenance of gene repression by the PRC2 complex is an important component of the imprinting mechanism in A. thaliana and other species. The PRC2 complex silences the hypomethylated maternal allele of PEGs, and the methylated paternal allele is expressed. Several studies have suggested that H3K9me2 and H3K27me3 are repressive marks that can substitute for one another in mutant contexts. We suggest that this substitution can also occur in wild-type tissues, and favour the hypothesis that in A. lyrata endosperm the maternal allele of at least a subset of PEGs is repressed by CHG methylation/H3K9me2. Overall, our results point to high conservation of imprinting accompanied by a distinct epigenetic signature, at least for PEGs. If the mechanism of imprinting is different but the genes that are imprinted are the same, this argues that imprinting is not simply a byproduct of endosperm methylation dynamics, but that imprinted expression of specific genes is under selection. Thus, the means by which monoallelic expression can be achieved are plastic, but the genes subject to this regulation are conserved.regions, but were additionally associated with gene body CHG hypermethylated DMRs in A. lyrata. Interestingly, gain of CHG methylation on the maternal allele was often accompanied by loss of CG gene body methylation, whereas paternally inherited alleles retained CG gene body methylation and had a similar methylation profile to embryo alleles (Fig. 4 and Supplementary Table 4). For the 22 PEGs lacking a gene body CHG hypermethylated DMR, half had a CG hypomethylated DMR in the flanking regions 2 kb 5′ or 3′, more like typical A. thaliana PEGs (Supplementary Table 4). Interestingly, these genes largely lacked CG gene body methylation in all tissues (Fig. 3a). Thus, there appear to be at least two classes of PEGs in terms of methylation features (Fig. 3a), which may correspond to different modes of epigenetic regulation. PEGs conserved with A. thaliana are found in both classes, although the majority (12/18) are CHG hypermethylated (Supplementary Table 4).To determine if there was a quantitative relationship between gain of CHG methylation and allelic expression bias, we plotted the difference in CHG methylation between maternal alleles in the embryo and endosperm relative to the ratio of maternal to paternal allele transcripts (Fig. 3c). The degree to which CHG methylation was gained on the maternal allele in endosperm relative to embryo was positively correlated with the extent of paternal allele expression bias in endosperm. In addition, PEG

Modelling lexical phrases acquisition in L2

The study focuses on the following points. It compares the views psycholinguists and computational linguists have concerning the processes of lexical access and lexical choice. Then it shows the similarities holding between the structure of the lexicon in L1 and in L2. It tries to offer a pedagogically realistic approach in vocabulary teaching based on these results

The Evolutionarily Conserved Longevity Determinants HCF-1 and SIR-2.1/SIRT1 Collaborate to Regulate DAF-16/FOXO

The conserved DAF-16/FOXO transcription factors and SIR-2.1/SIRT1 deacetylases are critical for diverse biological processes, particularly longevity and stress response; and complex regulation of DAF-16/FOXO by SIR-2.1/SIRT1 is central to appropriate biological outcomes. Caenorhabditis elegans Host Cell Factor 1 (HCF-1) is a longevity determinant previously shown to act as a co-repressor of DAF-16. We report here that HCF-1 represents an integral player in the regulatory loop linking SIR-2.1/SIRT1 and DAF-16/FOXO in both worms and mammals. Genetic analyses showed that hcf-1 acts downstream of sir-2.1 to influence lifespan and oxidative stress response in C. elegans. Gene expression profiling revealed a striking 80% overlap between the DAF-16 target genes responsive to hcf-1 mutation and sir-2.1 overexpression. Subsequent GO-term analyses of HCF-1 and SIR-2.1-coregulated DAF-16 targets suggested that HCF-1 and SIR-2.1 together regulate specific aspects of DAF-16-mediated transcription particularly important for aging and stress responses. Analogous to its role in regulating DAF-16/SIR-2.1 target genes in C. elegans, the mammalian HCF-1 also repressed the expression of several FOXO/SIRT1 target genes. Protein–protein association studies demonstrated that SIR-2.1/SIRT1 and HCF-1 form protein complexes in worms and mammalian cells, highlighting the conservation of their regulatory relationship. Our findings uncover a conserved interaction between the key longevity determinants SIR-2.1/SIRT1 and HCF-1, and they provide new insights into the complex regulation of FOXO proteins

Molecular and Clinical Characteristics in 46 Families Affected with Peutz-Jeghers Syndrome

Germline mutations of the tumor suppressor gene LKB1/STK11 are responsible for the Peutz-Jeghers syndrome (PJS), an autosomal-dominant disorder characterized by mucocutaneous pigmentation, hamartomatous polyps, and an increased risk of associated malignancies. In this study, we assessed the presence of pathogenic mutations in the LKB1/STK11 gene in 46 unrelated PJS families, and also carried genotype-phenotype correlation in regard of the development of cancer in 170 PJS patients belonging to these families. All LKB1/STK11 variants detected with single-strand conformational polymorphism were confirmed by direct sequencing, and those without LKB1/STK11 mutation were further submitted to Southern blot analysis for detection of deletions/rearrangements. Statistical analysis for genotype-phenotype correlation was performed. In 59% (27/46) of unrelated PJS cases, pathogenic mutations in the LKB1/STK11 gene, including 9 novel mutations, were identified. The new mutations were 2 splice site deletion-insertions, 2 missenses, 1 nonsense, and 4 abnormal splice sites. Genotype-phenotype analysis did not yield any significant differences between patients carrying mutations in LKB1/STK11 versus those without mutations, even with respect to primary biliary adenocarcinoma. This study presents the molecular characterization and cancer occurrence of a large cohort of PJS patients, increases the mutational spectrum of LKB1/STK11 allelic variants worldwide, and provides a new insight useful for clinical diagnosis and genetic counseling of PJS familie

Arabidopsis MORC proteins function in the efficient establishment of RNA directed DNA methylation.

The Microrchidia (MORC) family of ATPases are required for transposable element (TE) silencing and heterochromatin condensation in plants and animals, and C. elegans MORC-1 has been shown to topologically entrap and condense DNA. In Arabidopsis thaliana, mutation of MORCs has been shown to reactivate silent methylated genes and transposons and to decondense heterochromatic chromocenters, despite only minor changes in the maintenance of DNA methylation. Here we provide the first evidence localizing Arabidopsis MORC proteins to specific regions of chromatin and find that MORC4 and MORC7 are closely co-localized with sites of RNA-directed DNA methylation (RdDM). We further show that MORC7, when tethered to DNA by an artificial zinc finger, can facilitate the establishment of RdDM. Finally, we show that MORCs are required for the efficient RdDM mediated establishment of DNA methylation and silencing of a newly integrated FWA transgene, even though morc mutations have no effect on the maintenance of preexisting methylation at the endogenous FWA gene. We propose that MORCs function as a molecular tether in RdDM complexes to reinforce RdDM activity for methylation establishment. These findings have implications for MORC protein function in a variety of other eukaryotic organisms