Quantifying site-level usage and certainty of absence for an invasive species through occupancy analysis of camera-trap data

Efficient implementation of management programs for invasive species depends on accurate surveillance for guiding prioritization of surveillance and control resources in space and time. Occupancy probabilities can be used to determine where surveillance should occur. Conversely, knowledge of the certainty of site-level absence is of special interest in situations where the objective is to completely remove populations despite substantial risk of re-invasion. Indeed, the decision to shift from emphasizing control activities over the full range to emphasizing reinvasion prevention, surveillance, and response near the borders, depends on accurate knowledge of absence across space. We used a dynamic occupancy model to monitor changes in the distribution of an invasive species, feral swine (Sus scrofa), based on camera-trap data collected as part of a management program from June 2014 to January 2016 in San Diego County, California. Site usage of feral swine declined overall. The most informative predictors of site usage were spatial (latitude and longitude). Site-level non-usage rates increased over time and in response to management removal efforts; and site-level usage rates were heavily impacted by having neighboring sites that were used. Combining the detection probability estimated from the occupancy model and Bayes Theorem, we demonstrated how certainty of local (site-level) absence can be estimated iteratively in time in areas with negative surveillance (no detections) data. Our framework provides a means for using management-based surveillance data to quantify certainty of site-level absence of an invasive species, allowing for adaptive prioritization of surveillance and control resources. Our approach is flexible for application to other species and types of surveillance (e.g., track-plates, eDNA).     

Molecular evolution of mammalian lactate dehydrogenase-A genes and pseudogenes: association of a mouse processed pseudogene with a B1 repetitive sequence

A mouse genomic clone containing a lactate dehydrogenase-A (LDH-A) processed pseudogene and a B1 repetitive element was isolated, and a nucleotide sequence of approximately 3 kb was determined. The pseudogene and B1 element are flanked by perfect 13-bp repeats, and the B1 sequence starts at 14 nucleotides 3' to the presumptive polyadenylation signal of the pseudogene. The nucleotide sequences of the LDH-A genes and processed pseudogenes from mouse, rat, and human were compared, and a phylogenetic tree was constructed. The rate and pattern of nucleotide substitutions in the LDH-A pseudogenes are similar to previously reported results (Li et al. 1984). The average rate of nucleotide substitutions in the LDH-A pseudogenes is 4.3 X 10(- 9)/site/year. The substitutions of C----T and G----A are most frequent, and A----G substitutions are relatively high. The rate of synonymous substitutions in the LDH-A genes is 5.3 X 10(-9), which is not significantly higher than the average rate of 4.7 X 10(-9) for 35 mammalian genes. The rate of nonsynonymous substitutions in the LDH-A genes is 0.20 X 10(-9), which is considerably lower than the average rate of 0.88 X 10(-9) for 35 mammalian genes. Thus, the mammalian LDH-A gene appears to be highly conserved in evolution.      

3, 3′-diindolylmethane Enhances the Effectiveness of Herceptin against HER-2/Neu-Expressing Breast Cancer Cells

Herceptin failure is a major clinical problem in breast cancer. A subset of breast cancer patients with high HER-2/neu levels eventually experience metastatic disease progression when treated with Herceptin as a single agent. Mechanistic details of development of this aggressive disease are not clear. Therefore, there is a dire need to better understand the mechanisms by which drug resistance develops and to design new combined treatments that benefit patients with aggressive breast cancer and have minimal toxicity. We hypothesized that 3, 3′-diindolylmethane (DIM), a non-toxic agent can be combined with Herceptin to treat breast cancers with high levels of HER-2/neu. Here, we evaluated the effects of Herceptin alone and in combination with DIM on cell viability, apoptosis and clonogenic assays in SKBR3 (HER-2/neu-expressing) and MDA-MB-468 (HER-2/neu negative) breast cancer cells. We found that DIM could enhance the effectiveness of Herceptin by significantly reducing cell viability, which was associated with apoptosis-induction and significant inhibition of colony formation, compared with single agent treatment. These results were consistent with the down-regulation of Akt and NF-kB p65. Mechanistic investigations revealed a significant upregulation of miR-200 and reduction of FoxM1 expression in DIM and Herceptin-treated breast cancer cells. We, therefore, transfected cells with pre-miR-200 or silenced FoxM1 in these cells for understanding the molecular mechanism involved. These results provide experimental evidence, for the first time, that DIM plus Herceptin therapy could be translated to the clinic as a therapeutic modality to improve treatment outcome of patients with breast cancer, particularly for the patients whose tumors express high levels of HER-2/neu.     

Multiple duplications of yeast hexose transport genes in response to selection in a glucose-limited environment

When microbes evolve in a continuous, nutrient-limited environment, natural selection can be predicted to favor genetic changes that give cells greater access to limiting substrate. We analyzed a population of baker's yeast that underwent 450 generations of glucose-limited growth. Relative to the strain used as the inoculum, the predominant cell type at the end of this experiment sustains growth at significantly lower steady-state glucose concentrations and demonstrates markedly enhanced cell yield per mole glucose, significantly enhanced high-affinity glucose transport, and greater relative fitness in pairwise competition. These changes are correlated with increased levels of mRNA hybridizing to probe generated from the hexose transport locus HXT6. Further analysis of the evolved strain reveals the existence of multiple tandem duplications involving two highly similar, high- affinity hexose transport loci, HXT6 and HXT7. Selection appears to have favored changes that result in the formation of more than three chimeric genes derived from the upstream promoter of the HXT7 gene and the coding sequence of HXT6. We propose a genetic mechanism to account for these changes and speculate as to their adaptive significance in the context of gene duplication as a common response of microorganisms to nutrient limitation.      

In‐planta sporulation phenotype: a major life history trait to understand the evolution of Alnus‐infective Frankia strains

Two major types of Frankia strains are usually recognized, based on the ability to sporulate in‐planta: spore‐positive (Sp+) and spore‐negative (Sp?). We carried out a study of Sp+ and Sp? Frankia strains based on nodules collected on Alnus glutinosa, Alnus incana and Alnus viridis. The nodules were phenotyped using improved histology methods, and endophytic Frankia strain genotype was determined using a multilocus sequence analysis approach. An additional sampling was done to assess the relation between Sp+ phenotype frequency and genetic diversity of Frankia strains at the alder stand scale. Our results revealed that (i) Sp+ and Sp? Alnus‐infective Frankia strains are genetically different even when sampled from the same alder stand and the same host–plant species; (ii) there are at least two distinct phylogenetic lineages of Sp+ Frankia that cluster according to the host–plant species and without regard of geographic distance and (iii) genetic diversity of Sp+ strains is very low at the alder stand scale compared with Sp? strains. Difference in evolutionary history and genetic diversity between Sp+ and Sp? Frankia allows us to discuss the possible ecological role of in‐planta sporulation.     

Ecological drivers of African swine fever virus persistence in wild boar populations: Insight for control

Environmental sources of infection can play a primary role in shaping epidemiological dynamics; however, the relative impact of environmental transmission on host‐pathogen systems is rarely estimated. We developed and fit a spatially explicit model of African swine fever virus (ASFV) in wild boar to estimate what proportion of carcass‐based transmission is contributing to the low‐level persistence of ASFV in Eastern European wild boar. Our model was developed based on ecological insight and data from field studies of ASFV and wild boar in Eastern Poland. We predicted that carcass‐based transmission would play a substantial role in persistence, especially in low‐density host populations where contact rates are low. By fitting the model to outbreak data using approximate Bayesian computation, we inferred that between 53% and 66% of transmission events were carcass‐based that is, transmitted through contact of a live host with a contaminated carcass. Model fitting and sensitivity analyses showed that the frequency of carcass‐based transmission increased with decreasing host density, suggesting that management policies should emphasize the removal of carcasses and consider how reductions in host densities may drive carcass‐based transmission. Sensitivity analyses also demonstrated that carcass‐based transmission is necessary for the autonomous persistence of ASFV under realistic parameters. Autonomous persistence through direct transmission alone required high host densities; otherwise re‐introduction of virus periodically was required for persistence when direct transmission probabilities were moderately high. We quantify the relative role of different persistence mechanisms for a low‐prevalence disease using readily collected ecological data and viral surveillance data. Understanding how the frequency of different transmission mechanisms vary across host densities can help identify optimal management strategies across changing ecological conditions.