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Folate deficiency causes massive incorporation of uracil into human DNA (4 million per cell) and chromosome breaks. The likely mechanism is the deficient methylation of dUMP to dTMP and subsequent incorporation of uracil into DNA by DNA polymerase. During repair of uracil in DNA, transient nicks are formed; two opposing nicks could lead to chromosome breaks. Both high DNA uracil levels and elevated micronucleus frequency (a measure of chromosome breaks) are reversed by folate administration. A significant proportion of the U.S. population has low folate levels, in the range associated with elevated uracil misincorporation and chromosome breaks. Such breaks could contribute to the increased risk of cancer and cognitive defects associated with folate deficiency in humans

Se reporta el analisis del factor Bayes de un estudio reciente, para contrastar las hipótesis estadisticas, lo cual permite cuantificar una mayor evidencia contundente de la hipotesis de correlacion mas alla del tamaño de la muestra reducida, siendo asi un aporte metodológico en la investigación psicológica. The analysis of the Bayes factor of a recent study is reported, to contrast the statistical hypotheses, which allows quantifying a greater forceful evidence of the correlation hypothesis beyond the reduced sample size, being this way a methodological contribution in the psychological investigation. A análise do fator Bayes de um estudo recente é relatada, para contrastar as hipóteses estatísticas, o que permite quantificar uma evidência mais contundente da hipótese de correlação além do tamanho reduzido da amostra, sendo desta forma uma contribuição metodológica na investigação psicológica.

▪ Abstract  Methylation of cytosine residues in DNA provides a mechanism of gene control. There are two classes of methyltransferase in Arabidopsis; one has a carboxy-terminal methyltransferase domain fused to an amino-terminal regulatory domain and is similar to mammalian methyltransferases. The second class apparently lacks an amino-terminal domain and is less well conserved. Methylcytosine can occur at any cytosine residue, but it is likely that clonal transmission of methylation patterns only occurs for cytosines in strand-symmetrical sequences CpG and CpNpG. In plants, as in mammals, DNA methylation has dual roles in defense against invading DNA and transposable elements and in gene regulation. Although originally reported as having no phenotypic consequence, reduced DNA methylation disrupts normal plant development.

Little is known about the division of eukaryotic cell organelles and up to now neither in animals nor in plants has a gene product been shown to mediate this process. A cDNA encoding a homolog of the bacterial cell division protein FtsZ, an ancestral tubulin, was isolated from the eukaryote Physcomitrella patens and used to disrupt efficiently the genomic locus in this terrestrial seedless plant. Seven out of 51 transgenics obtained were knockout plants generated by homologous recombination; they were specifically impeded in plastid division with no detectable effect on mitochondrial division or plant morphology. Implications on the theory of endosymbiosis and on the use of reverse genetics in plants are discussed.

Grapevine fanleaf virus (GFLV), responsible for fanleaf degeneration, one of the most severe virus diseases of grapevines worldwide, causes substantial crop losses, reduces fruit quality and shortens longevity of grapevines. GFLV is transmitted from grapevine to grapevine by the ectoparasitic nematode Xiphinema index and belongs to genus Nepovirus, family Comoviridae. Since the discovery of the nematode vector in the late _50s and the identification of GFLV as the agent of fanleaf degeneration in the early _60s, a wealth of information was accumulated on its transmission, biological properties and serological characteristics, as well as on structure and expression of GFLV genome. Although dissemination of virus through propagation material has been drastically reduced over the past two decades by implementing rigorous certification schemes and establishing quarantine facilities, effective strategies are still needed to control GFLV in vineyards. Recently, significant progress has been made on the elucidation of the functions of most GFLV proteins, in particular the ones involved in critical steps of virus multiplication cycle, including RNA replication, cell-to-cell movement and transmission by X. index. New insights have also been gained into population structure and genomic variability among isolates from naturally infected vineyards, which have opened new pathways for designing alternative control strategies. This review article offers a comprehensive overview of the most significant advances made over the past 15 years on GFLV and discusses novel control strategies for one of the major threats to grapevine industry worldwide [Il Virus della foglia a ventaglio della vite (GFLV), responsabile della degenerazione a ventaglio, una delle più gravi malattie della vite a livello mondiale, causa rilevanti perdite produttive, riduce la qualità dell'uva e la longevità delle piante. Il GFLV viene trasmesso dal nematode ectoparassita Xiphinema index e appartiene al genere Nepovirus, famiglia Comoviridae. Dalla scoperta del vettore alla fine degli anni '50 e dall'identificazione del GFLV come agente della degenerazione a ventaglio nei primi anni '60, sono state accumulate molte informazioni su trasmissione, proprietà biologiche, caratteri sierologici e struttura ed espressione del genoma del GFLV. Sebbene la diffusione del virus col materiale di moltiplicazione sia stata ridotta drasticamente negli ultimi venti anni con rigorosi schemi di certificazione e strutture per la quarantena, sono tuttora necessarie strategie efficaci per il controllo del GFLV. Recentemente sono stati conseguiti progressi significativi sul chiarimento delle funzioni della maggior parte delle proteine del GFLV, in particolare quelle coinvolte nei passaggi critici del ciclo di moltiplicazione, comprendenti la replicazione dell'RNA, il movimento da cellula a cellula e la trasmissione tramite X. index. Sono state inoltre acquisite nuove informazioni sulla struttura e variabilità genomica delle popolazioni negli isolati provenienti da vigneti infetti naturalmente, che hanno aperto nuove strade per mettere a punto strategie di controllo alternative. Questa rassegna offre un panorama dei progressi più significativi conseguiti negli ultimi 15 anni sul GFLV e discute le strategie innovative di controllo di una delle maggiori minacce per la viticoltura mondiale]

Synergistic viral diseases of higher plants are caused by the interaction of two independent viruses in the same host and are characterized by dramatic increases in symptoms and in accumulation of one of the coinfecting viruses. In potato virus X (PVX)/potyviral synergism, increased pathogenicity and accumulation of PVX are mediated by the expression of potyviral 5' proximal sequences encoding P1, the helper component proteinase (HC-Pro), and a fraction of P3. Here, we report that the same potyviral sequence (termed P1/HC-Pro) enhances the pathogenicity and accumulation of two other heterologous viruses: cucumber mosaic virus and tobacco mosaic virus. In the case of PVX-potyviral synergism, we show that the expression of the HC-Pro gene product, but not the RNA sequence itself, is sufficient to induce the increase in PVX pathogenicity and that both P1 and P3 coding sequences are dispensable for this aspect of the synergistic interaction. In protoplasts, expression of the potyviral P1/HC-Pro region prolongs the accumulation of PVX (-) strand RNA and transactivates expression of a reporter gene from a PVX subgenomic promoter. Unlike the synergistic enhancement of PVX pathogenicity, which requires only expression of HC-Pro, the enhancement of PVX (-) strand RNA accumulation in protoplasts is significantly greater when the entire P1/HC-Pro sequence is expressed. These results indicate that the potyviral P1/HC-Pro region affects a step in disease development that is common to a broad range of virus infections and suggest a mechanism involving transactivation of viral replication

In wild-type diploid cells of Saccharomyces cerevisiae, an HO endonuclease-induced double-strand break (DSB) at the MAT locus can be efficiently repaired by gene conversion using the homologous chromosome sequences. Repair of the broken chromosome was nearly eliminated in rad52 delta diploids; 99% lost the broken chromosome. However, in rad51 delta diploids, the broken chromosomes were repaired approximately 35% of the time. None of these repair events were simple gene conversions or gene conversions with an associated crossover; instead, they created diploids homozygous for the MAT locus and all markers in the 100-kb region distal to the site of the DSB. In rad51 delta diploids, the broken chromosome can apparently be inherited for several generations, as many of these repair events are found as sectored colonies, with one part being repaired and the other part having lost the broken chromosome. Similar events occur in about 2% of wild-type cells. We propose that a broken chromosome end can invade a homologous template in the absence of RAD51 and initiate DNA replication that may extend to the telomere, 100 or more kb away. Such break-induced replication appears to be similar to recombination-initiated replication in bacteria

A quantitative and selective genetic assay was developed to monitor expansions of trinucleotide repeats (TNRs) in yeast. A promoter containing 25 repeats allows expression of a URA3 reporter gene and yields sensitivity to the drug 5-fluoroorotic acid. Expansion of the TNR to 30 or more repeats turns off URA3 and provides drug resistance. When integrated at either of two chromosomal loci, expansion rates were 1 x 10-5 to 4 x 10-5 per generation if CTG repeats were replicated on the lagging daughter strand. PCR analysis indicated that 5-28 additional repeats were present in 95% of the expanded alleles. No significant changes in CTG expansion rates occurred in strains deficient in the mismatch repair gene MSH2 or the recombination gene RAD52. The frequent nature of CTG expansions suggests that the threshold number for this repeat is below 25 in this system. In contrast, expansions of the complementary repeat CAG occurred at 500- to 1,000-fold lower rates, similar to a randomized (C,A,G) control sequence. When the reporter plasmid was inverted within the chromosome, switching the leading and lagging strands of replication, frequent expansions were observed only when CTG repeats resided on the lagging daughter strand. Among the rare CAG expansions, the largest gain in tract size was 38 repeats. The control repeats CTA and TAG showed no detectable rate of expansions. The orientation-dependence and sequence-specificity data support the model that expansions of CTG and CAG tracts result from aberrant DNA replication via hairpin-containing Okazaki fragments

Cdc7p is a protein kinase that is G1/S transition and initiation of DNA replication in Saccharomyces cerevisiae. The mechanisms whereby Cdc7p and its substrates exerts their effects are unknown. We report bite the characterization in S. cerevisiae of a recessive mutation in a member of the MCM family MCM5/CDC46, which bypasses the requirement for Cdc7p and its interacting factor Dbf4p. Because the MCM family of evolutionarily conserved proteins have been implicated in restricting DNA replication to once per cell cycle, our studies suggest that Cdc7p is required late in G1 because in its absence the Mcm5p/Cdc46p blocks the initiation of DNA replication. Moreover, Mcm5p/Cdc46p may have both positive and negative effects on the ability of cell to initiate replication

Telomerase is a specialized reverse transcriptase consisting of both RNA and protein components. Previous characterization of yeast telomerase function in vivo identified four EST (for ever shorter telomeres) genes that, when mutated, result in the phenotypes expected for a defect in telomerase. Consistent with this genetic prediction, the EST2 gene has recently been shown to encode the catalytic component of telomerase. Using an in vitro assay, we show here that telomerase activity is present in extracts prepared from yeast strains carrying est1-delta, est3-delta, and cdc13-2(est) mutations. Therefore, while these three genes are necessary for telomerase function in vivo, they do not encode components essential for core catalytic activity. When Est2p, the one EST gene product found to be essential for catalytic activity, was immunoprecipitated from extracts, the telomerase RNA subunit was also specifically precipitated, supporting the conclusion that these two components are in a stable complex