90 research outputs found

    The Vaccinia Virus Bifunctional Gene J3 (Nucleoside-2′-O-)-methyltransferase and Poly(A) Polymerase Stimulatory Factor Is Implicated as a Positive Transcription Elongation Factor by Two Genetic Approaches

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    AbstractVaccinia virus genes A18 and G2 affect the elongation and termination of postreplicative viral gene transcription in opposite ways. Viruses with mutations in gene A18 produce abnormally long transcripts, indicating that A18 is a negative transcription elongation factor. Viruses containing mutations in gene G2 produce transcripts that are abnormally short, truncated specifically from their 3′ ends, indicating that G2 is a positive transcription elongation factor. Despite the fact that both A18 and G2 are essential genes, A18-G2 double-mutant viruses are viable, presumably because the effects of the mutations are mutually compensatory. In addition, the anti-poxviral drug isatin-β-thiosemicarbazone (IBT) seems to enhance elongation during a vaccinia infection: IBT treatment of a wildtype vaccinia infection induces a phenotype identical to an A18 mutant infection, and G2 mutant viruses are dependent on IBT for growth, presumably because IBT restores the G2 mutant truncated transcripts to a normal length. These observations inspire two independent genetic selections that have now been used to identify an additional vaccinia gene, J3, that regulates postreplicative transcription elongation. In the first selection, a single virus that contains an extragenic suppressor of the A18 temperature-sensitive mutant, Cts23, was isolated. In the second selection, several spontaneous IBT-dependent (IBTd) mutant viruses were isolated and characterized genetically. Marker rescue mapping and DNA sequence analysis show that the extragenic suppressor of Cts23 contains a point mutation in the J3 gene, while each of seven new IBTd mutants contains null mutations in the J3 gene. The J3 protein has previously been identified as a (nucleoside-2′-O-)-methyltransferase and as a processivity subunit for the heterodimeric viral poly(A) polymerase. The nature of the two independent selections used to isolate the J3 mutants strongly suggests that the J3 protein serves as a positive postreplicative transcription elongation factor during a normal virus infection

    Interaction between the J3R Subunit of Vaccinia Virus Poly(A) Polymerase and the H4L Subunit of the Viral RNA Polymerase

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    AbstractJ3R, the 39-kDa subunit of vaccinia virus poly(A) polymerase, is a multifunctional protein that catalyzes (nucleoside-2′-O-)-methyltransferase activity, serves as a poly(A) polymerase stimulatory factor, and acts as a postreplicative positive transcription elongation factor. Prior results support an association between poly(A) polymerase and the virion RNA polymerase. A possible direct interaction between J3R and H4L subunit of virion RNA polymerase was evaluated. J3R was shown to specifically bind to H4L amino acids 235–256, C terminal to NPH I binding site on H4L. H4L binds to the C-terminal region of J3R between amino acids 169 and 333. The presence of a J3R binding site near to the NPH I binding region on H4L led us to evaluate a physical interaction between NPH I and J3R. The NPH I binding site was located on J3R between amino acids 169 and 249, and J3R was shown to bind to NPH I between amino acids 457 and 524. To evaluate a role for J3R in early gene mRNA synthesis, transcription termination, and/or release, a transcription-competent extract prepared from cells infected with mutant virus lacking J3R, J3-7. Analysis of transcription activity demonstrated that J3R is not required for early mRNA synthesis and is not an essential factor in early gene transcription termination or transcript release in vitro. J3R interaction with NPH I and H4L may serve as a docking site for J3R on the virion RNA polymerase, linking transcription to mRNA cap formation and poly(A) addition

    the american naturalist

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    One main goal of forest ecology is to infer past changes and predict future changes in species composition, and examining the diameter distributions of canopy species is often used toward this end Theory indicates that higher rates of population change, λ, lead to the process of being eliminated from the forest-perhaps more steeply declining size distributions (more juveniles relative during succession-fail to reproduce and thus lack sufto adults). But other parameters also affect the size distribution: ficient advanced regeneration. ''The lack of congruence lower growth rate of juveniles and lower survival at any size pro-between overstory and understory in these stands is both duce more steeply declining size distributions as well. Empirical an indicator of change as well as a major concern for evaluation of 216 tree populations showed that juvenile growth conservation' ' (Foster et al. 1996, p. 420). In the tropics, was the strongest predictor of size distribution, in the direction the use of diameter distributions to project community predicted by theory. Size distribution did correlate with population growth, but weakly and only in understory species, not canopy change has been especially important in Africa, and sevspecies. Size distribution did not correlate with the growth rate of eral early studies suggested that dominant canopy species larger individuals nor with survival. Results suggest that static in-in African forests do not produce juveniles in the immeformation on the size distribution is not a good predictor of future diate area. This led to the idea of cyclical succession, or population trends, while demographic information is. Fast-grow-the mosaic theory of regeneration provide in-depth analyses of these ideas, using extensive quantitative data on size distributions. But the underlying assumption-that populations with low juvenile density relative to adult density are in deEcologists often use size distribution to indicate the cline-has not been explicitly tested. Here we address health of a population. If there are large numbers of ju-two ways of making this test. We first employ a theoretical approach, examining quantitative population models * E-mail: [email protected]. to determine how size distribution relates to population † E-mail: [email protected]. growth. Then we proceed with a direct, empirical test us- ‡ E-mail: [email protected]. ing records of population change over 13 yr in a tree § E-mail: [email protected]. community. In all 216 species abundant enough to ana

    Demographic trade-offs predict tropical forest dynamics

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    Understanding tropical forest dynamics and planning for their sustainable management require efficient, yet accurate, predictions of the joint dynamics of hundreds of tree species. With increasing information on tropical tree life histories, our predictive understanding is no longer limited by species data but by the ability of existing models to make use of it. Using a demographic forest model, we show that the basal area and compositional changes during forest succession in a neotropical forest can be accurately predicted by representing tropical tree diversity (hundreds of species) with only five functional groups spanning two essential trade-offs—the growth-survival and stature-recruitment trade-offs. This data-driven modeling framework substantially improves our ability to predict consequences of anthropogenic impacts on tropical forests

    Growth Strategies of Tropical Tree Species: Disentangling Light and Size Effects

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    An understanding of the drivers of tree growth at the species level is required to predict likely changes of carbon stocks and biodiversity when environmental conditions change. Especially in species-rich tropical forests, it is largely unknown how species differ in their response of growth to resource availability and individual size. We use a hierarchical Bayesian approach to quantify the impact of light availability and tree diameter on growth of 274 woody species in a 50-ha long-term forest census plot in Barro Colorado Island, Panama. Light reaching each individual tree was estimated from yearly vertical censuses of canopy density. The hierarchical Bayesian approach allowed accounting for different sources of error, such as negative growth observations, and including rare species correctly weighted by their abundance. All species grew faster at higher light. Exponents of a power function relating growth to light were mostly between 0 and 1. This indicates that nearly all species exhibit a decelerating increase of growth with light. In contrast, estimated growth rates at standardized conditions (5 cm dbh, 5% light) varied over a 9-fold range and reflect strong growth-strategy differentiation between the species. As a consequence, growth rankings of the species at low (2%) and high light (20%) were highly correlated. Rare species tended to grow faster and showed a greater sensitivity to light than abundant species. Overall, tree size was less important for growth than light and about half the species were predicted to grow faster in diameter when bigger or smaller, respectively. Together light availability and tree diameter only explained on average 12% of the variation in growth rates. Thus, other factors such as soil characteristics, herbivory, or pathogens may contribute considerably to shaping tree growth in the tropics

    Does Sex Speed Up Evolutionary Rate and Increase Biodiversity?

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    Most empirical and theoretical studies have shown that sex increases the rate of evolution, although evidence of sex constraining genomic and epigenetic variation and slowing down evolution also exists. Faster rates with sex have been attributed to new gene combinations, removal of deleterious mutations, and adaptation to heterogeneous environments. Slower rates with sex have been attributed to removal of major genetic rearrangements, the cost of finding a mate, vulnerability to predation, and exposure to sexually transmitted diseases. Whether sex speeds or slows evolution, the connection between reproductive mode, the evolutionary rate, and species diversity remains largely unexplored. Here we present a spatially explicit model of ecological and evolutionary dynamics based on DNA sequence change to study the connection between mutation, speciation, and the resulting biodiversity in sexual and asexual populations. We show that faster speciation can decrease the abundance of newly formed species and thus decrease long-term biodiversity. In this way, sex can reduce diversity relative to asexual populations, because it leads to a higher rate of production of new species, but with lower abundances. Our results show that reproductive mode and the mechanisms underlying it can alter the link between mutation, evolutionary rate, speciation and biodiversity and we suggest that a high rate of evolution may not be required to yield high biodiversity

    Direct and indirect effects of climate on richness drive the latitudinal diversity gradient in forest trees

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    Data accessibility statement: Full census data are available upon reasonable request from the ForestGEO data portal, http://ctfs.si.edu/datarequest/ We thank Margie Mayfield, three anonymous reviewers and Jacob Weiner for constructive comments on the manuscript. This study was financially supported by the National Key R&D Program of China (2017YFC0506100), the National Natural Science Foundation of China (31622014 and 31570426), and the Fundamental Research Funds for the Central Universities (17lgzd24) to CC. XW was supported by the Strategic Priority Research Program of the Chinese Academy of Sciences (XDB3103). DS was supported by the Czech Science Foundation (grant no. 16-26369S). Yves Rosseel provided us valuable suggestions on using the lavaan package conducting SEM analyses. Funding and citation information for each forest plot is available in the Supplementary Information Text 1.Peer reviewedPostprin
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