Posttranscriptional gene silencing (PTGS), or RNA silencing, is a sequence-specific RNA degradation process that targets foreign RNA, including viral and transposon RNA for destruction. Several RNA plant viruses have been shown to encode suppressors of PTGS in order to survive this host defense. We report here that the coat protein (CP) of Turnip crinkle virus (TCV) strongly suppresses PTGS. The Agrobacterium infiltration system was used to demonstrate that TCV CP suppressed the local PTGS as strongly as several previously reported virus-coded suppressors and that the action of TCV CP eliminated the small interfering RNAs associated with PTGS. We have also shown that the TCV CP must be present at the time of silencing initiation to be an effective suppressor. TCV CP was able to suppress PTGS induced by sense, antisense, and doublestranded RNAs, and it prevented systemic silencing. These data suggest that TCV CP functions to suppress RNA silencing at an early initiation step, likely by interfering the function of the Dicer-like RNase in plants.Posttranscriptional gene silencing (PTGS) is a sequencespecific RNA degradation process that leads to the elimination of the targeted RNA and loss of the function(s) encoded by the targeted RNA (1,6,62,69). This phenomenon was first observed and intensively studied in plant systems (see reference 64 for a review), where it has been associated with several processes, including cosuppression (44), repeat induced gene silencing (70), RNA-mediated resistance (35, 58), or homology-dependent gene silencing (43). Similar mechanisms were later discovered in other organisms, including quelling in filamentous fungus Neurospora crassa (9) and RNA interference (RNAi) in Caenorhabditis elegans (18) and Drosophila melanogaster (30). Recent research has revealed that all of these different phenomena have many common features and are now considered to be manifestations of an RNA-targeting pathway, whose natural functions include protecting hosts from invading viral RNAs and transposons (see references 45, 54, and 72 for reviews). RNA silencing has been proposed as a more general term to describe these related processes (1).Initiation and maintenance stages have been identified as distinct phases of the PTGS or RNA silencing process (10,50,65). In the initiation stage, the invading RNA triggers a pathway that results in its being degraded into a small RNA species of discrete size (21 to 25 nucleotides [nt]) called small interfering RNAs (siRNAs) that function as a guide for further degradation in the maintenance stage (22, 71). The most potent initiator of PTGS is thought to be double-stranded RNA (dsRNA) (8,18,30,68), although single-stranded RNA (ssRNA), both sense and antisense orientations, or even DNA trigger RNA silencing (15,65,66). ssRNA is most likely converted to a double-stranded form with the help of a host RNAdependent RNA polymerase (RdRP) in order to be effective (9,11,42,52,57). The dsRNA initiators are then degraded by an RNase III-like RNase (e.g., Dicer in Drosophila [3])...
ATR-X (alpha thalassemia/mental retardation, X-linked) syndrome is a human congenital disorder that causes severe intellectual disabilities. Mutations in the ATRX gene, which encodes an ATP-dependent chromatin-remodeler, are responsible for the syndrome. Approximately 50% of the patient missense mutations are clustered in a cysteine-rich domain termed ADD (ATRX-DNMT3-DNMT3L, AD-DATRX), indicating its importance. However, the function of ADDATRX has remained elusive. Here we identify ADDATRX as a novel histone H3 binding module, whose binding is promoted by lysine 9 trimethylation (H3K9me3) but inhibited by H3K4me3. The co-crystal structures of ADDATRX bound to H31–15K9me3 peptide reveals an atypical composite H3K9me3-binding pocket, which is distinct from the conventional trimethyllysine-binding aromatic cage. Importantly, H3K9me3-pocket mutants and ATR-X syndrome mutants are defective in both H3K9me3 binding and localization at pericentromeric heterochromatin. Thus, we have discovered a unique histone recognition mechanism underlying the ATR-X etiology.
Using three different assays, we examined 103 serum samples collected from different civet farms and a market in China in June 2003 and January 2004. While civets on farms were largely free from SARS-CoV infection, ≈80% of the animals from one animal market in Guangzhou contained significant levels of antibody to SARS-CoV, which suggests no widespread infection among civets resident on farms, and the infection of civets in the market might be associated with trading activities under the conditions of overcrowding and mixing of various animal species.
Rye is a valuable food and forage crop, an important genetic resource for wheat and triticale improvement and an indispensable material for efficient comparative genomic studies in grasses. Here, we sequenced the genome of Weining rye, an elite Chinese rye variety. The assembled contigs (7.74 Gb) accounted for 98.47% of the estimated genome size (7.86 Gb), with 93.67% of the contigs (7.25 Gb) assigned to seven chromosomes. Repetitive elements constituted 90.31% of the assembled genome. Compared to previously sequenced Triticeae genomes, Daniela, Sumaya and Sumana retrotransposons showed strong expansion in rye. Further analyses of the Weining assembly shed new light on genome-wide gene duplications and their impact on starch biosynthesis genes, physical organization of complex prolamin loci, gene expression features underlying early heading trait and putative domestication-associated chromosomal regions and loci in rye. This genome sequence promises to accelerate genomic and breeding studies in rye and related cereal crops.
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