Convergence or redundancy: alternative views about the evolutionary genomics of character displacement.

An evolutionary debate contrasts the importance of genetic convergence versus genetic redundancy. In genetic convergence, the same adaptive trait evolves because of similar genetic changes. In genetic redundancy, the adaptive trait evolves using different genetic combinations, and populations might not share the same genetic changes. Here we address this debate by examining single nucleotide polymorphisms (SNPs) associated with the rapid evolution of character displacement in Anolis carolinensis populations inhabiting replicate islands with and without a competitor species (1Spp and 2Spp islands, respectively). We identify 215-outliers SNPs that have improbably large FST values, low nucleotide variation, greater linkage than expected and that are enriched for genes underlying animal movement. The pattern of SNP divergence between 1Spp and 2Spp populations supports both genetic convergence and genetic redundancy for character displacement. In support of genetic convergence: all 215-outliers SNPs are shared among at least three of the five 2Spp island populations, and 23% of outlier SNPS are shared among all five 2Spp island populations. In contrast, in support of genetic redundancy: many outlier SNPs only have meaningful allele frequency differences between 1Spp and 2Spp islands on a few 2Spp islands. That is, on at least one of the 2Spp islands, 77% of outlier SNPs have allele frequencies more similar to those on 1Spp islands than to those on 2Spp islands. Focusing on genetic convergence is scientifically rigorous because it relies on replication. Yet, this focus distracts from the possibility that there are multiple, redundant genetic solutions that enhance the rate and stability of adaptive change.

The green peach aphid gut contains host plant microRNAs identified by comprehensive annotation of Brassica oleracea small RNA data.

Like all organisms, aphids, plant sap-sucking insects that house a bacterial endosymbiont called Buchnera, are members of a species interaction network. Ecological interactions across such networks can result in phenotypic change in network members mediated by molecular signals, like microRNAs. Here, we interrogated small RNA data from the aphid, Myzus persicae, to determine the source of reads that did not map to the aphid or Buchnera genomes. Our analysis revealed that the pattern was largely explained by reads that mapped to the host plant, Brassica oleracea, and a facultative symbiont, Regiella. To start elucidating the function of plant small RNA in aphid gut, we annotated 213 unique B. oleracea miRNAs; 32/213 were present in aphid gut as mature and star miRNAs. Next, we predicted targets in the B. oleracea and M. persicae genomes for these 32 plant miRNAs. We found that plant targets were enriched for genes associated with transcription, while the distribution of targets in the aphid genome was similar to the functional distribution of all genes in the aphid genome. We discuss the potential of plant miRNAs to regulate aphid gene expression and the mechanisms involved in processing, export and uptake of plant miRNAs by aphids.

Aggregated and Hyperstable Damage-Associated Molecular Patterns Are Released During ER Stress to Modulate Immune Function.

Chronic ER stress occurs when protein misfolding in the Endoplasmic reticulum (ER) lumen remains unresolved despite activation of the unfolded protein response. We have shown that traumatic injury such as a severe burn leads to chronic ER stress in vivo leading to systemic inflammation which can last for more than a year. The mechanisms linking chronic ER stress to systemic inflammatory responses are not clear. Here we show that induction of chronic ER stress leads to the release of known and novel damage-associated molecular patterns (DAMPs). The secreted DAMPs are aggregated and markedly protease resistant. ER stress-derived DAMPs activate dendritic cells (DCs) which are then capable of polarizing naïve T cells. Our findings indicate that induction of chronic ER stress may lead to the release of hyperstable DAMPs into the circulation resulting in persistent systemic inflammation and adverse outcomes.