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Epigenetic mechanisms may play a central role in mediating phenotypic plasticity, especially during range expansions, when populations face a suite of novel environmental conditions. Individuals may differ in their epigenetic potential (EP; their capacity for epigenetic modifications of gene expression), which may affect their ability to colonize new areas. One form of EP, the number of CpG sites, is higher in introduced house sparrows (Passer domesticus) than in native birds in the promoter region of a microbial surveillance gene, Toll-like Receptor 4 (TLR4), which may allow invading birds to fine-tune their immune responses to unfamiliar parasites. Here, we compared TLR4 gene expression from whole blood, liver and spleen in house sparrows with different EP, first challenging some birds with lipopolysaccharide (LPS), to increase gene expression by simulating a natural infection. We expected that high EP would predict high inducibility and reversibility of TLR4 expression in the blood of birds treated with LPS, but we did not make directional predictions regarding organs, as we could not repeatedly sample these tissues. We found that EP was predictive of TLR4 expression in all tissues. Birds with high EP expressed more TLR4 in the blood than individuals with low EP, regardless of treatment with LPS. Only females with high EP exhibited reversibility in gene expression. Further, the effect of EP varied between sexes and among tissues. Together, these data support EP as one regulator of TLR4 expression.

 

Changes in vegetation productivity based on normalized difference vegetation index (NDVI) have been reported from Arctic regions. Most studies use very coarse spatial resolution remote sensing data that cannot isolate landscape level factors. For example, on Yamal Peninsula in West Siberia enhanced willow growth has been linked to widespread landslide activity, but the effect of landslides on regional NDVI dynamics is unknown. Here we apply a novel satellite-based NDVI analysis to investigate the vegetation regeneration patterns of active-layer detachments following a major landslide event in 1989. We analyzed time series data of Landsat and very high-resolution (VHR) imagery from QuickBird-2 and WorldView-2 and 3 characterizing a study area of ca. 35 km². Landsat revealed that natural regeneration of low Arctic tundra progressed rapidly during the first two decades after the landslide event. However, during the past decade, the difference between landslide shear surfaces and surrounding areas remained relatively unchanged despite the advance of vegetation succession. Time series also revealed that NDVI generally declined since 2013 within the study area. The VHR imagery allowed detection of NDVI change ‘hot-spots’ that included temporary degradation of vegetation cover, as well as new and expanding thaw slumps, which were too small to be detected from Landsat satellite data. Our study demonstrates that landslides can have pronounced and long-lasting impacts on tundra vegetation. Thermokarst landslides and associated impacts on vegetation will likely become increasingly common in NW Siberia and other Arctic regions with continued warming.

 

DNA methylation is an epigenetic modification with wide-ranging consequences across the life of an organism. This modification can be stable, persisting through development despite changing environmental conditions. However, in other contexts, DNA methylation can also be flexible, underlying organismal phenotypic plasticity. One underappreciated aspect of DNA methylation is that it is a potent mutagen; methylated cytosines mutate at a much faster rate than other genetic motifs. This mutagenic property of DNA methylation has been largely ignored in eco-evolutionary literature, despite its prevalence. Here, we explore how DNA methylation induced by environmental and other factors could promote mutation and lead to evolutionary change at a more rapid rate and in a more directed manner than through stochastic genetic mutations alone. We argue for future research on the evolutionary implications of DNA methylation driven mutations both within the lifetime of organisms, as well as across timescales.

 

ABSTRACT Quantifying the relative importance of genomic and epigenomic modulators of phenotype is a focal challenge in comparative physiology, but progress is constrained by availability of data and analytic methods. Previous studies have linked physiological features to coding DNA sequence, regulatory DNA sequence, and epigenetic state, but few have disentangled their relative contributions or unambiguously distinguished causative effects (‘drivers’) from correlations. Progress has been limited by several factors, including the classical approach of treating continuous and fluid phenotypes as discrete and static across time and environment, and difficulty in considering the full diversity of mechanisms that can modulate phenotype, such as gene accessibility, transcription, mRNA processing and translation. We argue that attention to phenotype nuance, progressing to association with epigenetic marks and then causal analyses of the epigenetic mechanism, will enable clearer evaluation of the evolutionary path. This would underlie an essential paradigm shift, and power the search for links between genomic and epigenomic features and physiology. Here, we review the growing knowledge base of gene-regulatory mechanisms and describe their links to phenotype, proposing strategies to address widely recognized challenges.