8 research outputs found

    The Last Trees Standing: Climate modulates tree survival factors during a prolonged bark beetle outbreak in Europe

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    Plant traits are an expression of strategic tradeoffs in plant performance that determine variation in allocation of finite resources to alternate physiological functions. Climate factors interact with plant traits to mediate tree survival. This study investigated survival dynamics in Norway spruce (Picea abies) in relation to tree-level morphological traits during a prolonged multi-year outbreak of the bark beetle, Ips typographus, in Central Europe. We acquired datasets describing the trait attributes of individual spruce using remote sensing and field surveys. We used nonlinear regression in a hypothesis-driven framework to quantify survival probability as a function of tree size, crown morphology, intraspecific competition and a growing season water balance. Extant spruce trees that persisted through the outbreak were spatially clustered, suggesting that survival was a nonrandom process. Larger diameter trees were more susceptible to bark beetles, reflecting either life history tradeoffs or a dynamic interaction between defense capacity and insect aggregation behavior. Competition had a strong negative effect on survival, presumably through resource limitation. Trees with more extensive crowns were buffered against bark beetles, ostensibly by a more robust photosynthetic capability and greater carbon reserves. The outbreak spanned a warming trend and conditions of anomalous aridity. Sustained water limitation during this period amplified the consequences of other factors, rendering even smaller trees vulnerable to colonization by insects. Our results are in agreement with prior research indicating that climate change has the potential to intensify bark beetle activity. However, forest outcomes will depend on complex cross-scale interactions between global climate trends and tree-level trait factors, as well as feedback effects associated with landscape patterns of stand structural diversity

    Interaction of HIF and USF signaling pathways at human genes flanked by hypoxia-response elements and E-box palindromes

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    Rampant activity of the hypoxia-inducible factor (HIF)-1 in cancer is frequently associated with the malignant progression into a harder-to-treat, increasingly aggressive phenotype. Clearly, anti-HIF strategies in cancer cells are of considerable clinical interest. One way to fine-tune, or inhibit, HIF's transcriptional outflow independently of hydroxylase activities could be through competing transcription factors. A CACGTG-binding activity in human hepatoma cells was previously found to restrict HIF's access to hypoxia response cis-elements (HRE) in a Daphnia globin gene promoter construct (phb2). The CACGTG factor, and its impact on hypoxia-responsive human genes, was analyzed in this study by genome-wide computational scans as well as gene-specific quantitative PCR, reporter and DNA-binding assays in hepatoma (Hep3B), cervical carcinoma (HeLa), and breast carcinoma (MCF7) cells. Among six basic helix-loop-helix transcription factors known to target CACGTG palindromes, we identified upstream stimulatory factor (USF)-1/2 as predominant phb2 CACGTG constituents in Hep3B, HeLa, and MCF7 cells. Human genes with adjacent or overlapping HRE and CACGTG motifs included with lactate dehydrogenase A (LDHA) and Bcl-2/E1B 19 kDa interacting protein 3 (BNIP3) hypoxia-induced HIF-1 targets. Parallel recruitment of HIF-1α and USF1/2a to the respective promoter chromatin was verified for all cell lines investigated. Mutual complementing (LDHA) or moderating (BNIP3) cross-talk was seen upon overexpression or silencing of HIF-1α and USF1/2a. Distinct (LDHA) or overlapping (BNIP3) promoter-binding sites for HIF-1 and USFs were subsequently characterized. We propose that, depending on abundance or activity of its protein constituents, O(2)-independent USF signaling can function to fine-tune or interfere with HIF-mediated transcription in cancer cells. Mol Cancer Res; 1-17. ©2011 AACR

    Comparative genome sequencing of Drosophila pseudoobscura: Chromosomal, gene, and cis-element evolution

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    We have sequenced the genome of a second Drosophila species, Drosophila pseudoobscura, and compared this to the genome sequence of Drosophila melanogaster, a primary model organism. Throughout evolution the vast majority of Drosophila genes have remained on the same chromosome arm, but within each arm gene order has been extensively reshuffled, leading to a minimum of 921 syntenic blocks shared between the species. A repetitive sequence is found in the A pseudoobscura genome at many junctions between adjacent syntenic blocks. Analysis of this novel repetitive element family suggests that recombination between offset elements may have given rise to many paracentric inversions, thereby contributing to the shuffling of gene order in the D. pseudoobscura lineage. Based on sequence similarity and synteny, 10,516 putative orthologs have been identified as a core gene set conserved over 25-55 million years (Myr) since the pseudoobscura/melanogaster divergence. Genes expressed in the testes had higher amino acid sequence divergence than the genome-wide average, consistent with the rapid evolution of sex-specific proteins. Cis-regulatory sequences are more conserved than random and nearby sequences between the species-but the difference is slight, suggesting that the evolution of cis-regulatory elements is flexible. Overall, a pattern of repeat-mediated chromosomal rearrangement, and high coadaptation of both male genes and cis-regulatory sequences emerges as important themes of genome divergence between these species of Drosophila
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