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Thompson, V.

Publications and source records attributed to Thompson, V..

3 recordsLinked to original sources

One species, two lives: cryptic population structure and life-history divergence in a vineyard spittlebug (Aphrophora sp.), a candidate vector for Pierce's disease

Whole genome analysis of spittlebug populations, an Aphrophora species (Hemiptera: Aphrophoridae) known to spread Pierce's disease, from various vineyards in Napa and Sonoma Counties demonstrates that these insects are conspecific with Aphrophora permutata found in quasi-natural populations. The genomes analyzed fall in three autosomal clusters with two sympatric populations (based on admixture) that diverged around 40,000-90,000 years before present according to demographic models. We also recover three related but distinct mitochondrial clusters. There is no genetic differentiation between Napa and Sonoma County vineyard populations and very modest differentiation among vineyards and quasi-natural Berkeley/Oakland Hills population. These vineyard and quasi-natural populations have distinct life histories, including divergent oviposition hosts (understory herbs versus pines) and different patterns of adult seasonal migration (out-migration and return versus simple movement from the understory to the pine canopy). Analysis of the mitochondrial gene COI indicates that A. permutata, Aphrophora fulva and Aphrophora maculosa are intermingled in the same mitochondrial clade, along with the more distantly related species Aphrophora gelida. Further, all three autosomal genetic clusters show evidence of selection for insecticide resistance. We also find that endosymbionts Wolbachia and Rickettsia were both present in a substantial fraction of specimens analyzed, but neither appears to influence population structure. Overall, our findings elucidate an intriguing degree of life history divergence between geographically proximate, conspecific populations linked by gene flow and may have implications for the continued management of vineyard populations.

ecology↗

Wolbachia in the spittlebug Prosapia ignipectus: Variable infection frequencies, but no apparent effect on host reproductive isolation

Animals serve as hosts for complex communities of microorganisms, including endosymbionts that live inside their cells. Wolbachia bacteria are perhaps the most common endosymbionts, manipulating host reproduction to propagate. Many Wolbachia cause intense cytoplasmic incompatibility (CI) that promotes their spread to high and relatively stable frequencies. Wolbachia that cause weak or no CI tend to persist at intermediate, often variable, frequencies. Wolbachia could also contribute to host reproductive isolation (RI), although current support for such contributions is limited to a few systems. To test for Wolbachia frequency variation and effects on host RI, we sampled several local Prosapia ignipectus (Fitch)(Hemiptera: Cercopidae) spittlebug populations in the northeastern USA over two years, including closely juxtaposed Maine populations with different monomorphic color forms, "black" and "lined". We discovered a group-B Wolbachia (wPig) infecting P. ignipectus that diverged from group-A Wolbachia--like model wMel and wRi strains in Drosophila--6 to 46 MYA. Populations of the sister species Prosapia bicincta (Say) from Hawaii and Florida are uninfected, suggesting that P. ignipectus acquired wPig after their initial divergence. wPig frequencies were generally high and variable among sites and between years. While phenotyping wPig effects on host reproduction is not currently feasible, the wPig genome contains three divergent sets of CI loci, consistent with high wPig frequencies. Finally, Maine monomorphic black and monomorphic lined populations of P. ignipectus share both wPig and mtDNA haplotypes, implying no apparent effect of wPig on the maintenance of this morphological contact zone. We hypothesize P. ignipectus acquired wPig horizontally as observed for many Drosophila species, and that significant CI and variable transmission produce high but variable wPig frequencies.

evolutionary biology↗

Obesity-Activated Lung Stomal Cells Promote Myeloid-Lineage Cell Accumulation and Breast Cancer Metastasis

Obesity is correlated with increased incidence of breast cancer metastasis, however the mechanisms underlying how obesity promotes metastasis are unclear. In a diet-induced obesity mouse model, obesity enhanced lung metastases in both the presence and absence of primary mammary tumors and increased recruitment of myeloid lineage cells into the lungs. In the absence of tumors, obese mice demonstrated increased numbers of myeloid lineage cells and elevated collagen fibers within the lung stroma, reminiscent of pre-metastatic niches formed by primary tumors. Lung stromal cells isolated from obese non-tumor-bearing mice showed increased proliferation, contractility, and expression of extracellular matrix, inflammatory markers, and TGF{beta}1. Conditioned media from lung stromal cells from obese mice promoted myeloid lineage cell migration in vitro in response to CSF2 expression and enhanced invasion of tumor cells. Together, these results suggest that prior to tumor formation, obesity alters the lung microenvironment, creating niches conducive for metastatic growth.

cancer biology↗