Tactics to Stay Alive: Predation Risk Alters Body Condition and Escape Behaviour

Recent manipulations show that when perceived predation risk is high, animals will chronically alter their escape behaviour, even if it affects physiological condition to such an extent that survival may be reduced. I tested the relationships amongst predation risk, mass change, and flying capacity in brown-headed cowbirds (Molothrus ater) housed in large outdoor aviaries. I measured changes in the birds’ body condition, take-off behaviour and flying capacity after manipulating the ambient level of perceived predation risk in their environment using various predator or non-predator cues. Cowbirds exposed to predator stimuli gained, rather than lost, body mass and changed their take-off behaviour, by flying at higher angles and reduced speeds. Critically, flying capacity was not affected by any of these changes. I suggest these responses may be anti-predator tactics that birds utilize to reduce starvation risk and improve their chances of predator evasion when predation risk is high

Too important to tamper with: predation risk affects body mass and escape behaviour but not escape ability

Escaping from a predator is a matter of life or death, and prey are expected to adaptively alter their physiology under chronic predation risk in ways that may affect escape. Theoretical models assume that escape performance is mass dependent, whereby scared prey strategically maintain an optimal body mass to enhance escape. Experiments testing the mass-dependent predation risk hypothesis have demonstrated that prior experience of predation risk can affect body mass, and the behavioural decisions about evasive actions to take. Other studies on natural changes in body mass indicate that mass can affect escape. No single experiment has tested if all of these components are indeed linked, which is a critical necessary condition underpinning the mass-dependent predation risk hypothesis. We tested all components of the mass-dependent predation risk hypothesis in a repeated measures experiment by presenting predator and non-predator cues to brown-headed cowbirds housed in semi-natural conditions. Exposure to predator cues affected body mass, fat, pectoral muscle thickness and evasive actions (take-off angle and speed), but not the physiological capacity to escape, as measured by flying ability. Examining individual variation revealed that flying ability was unrelated to mass loss in either sex, unrelated to mass gain in males, and only females that gained a very large amount of mass flew poorly. We next conducted a body mass manipulation in the laboratory to rigorously test whether small to large perturbations in mass can ever affect flying ability. We induced either no change in mass (control), a moderate reduction of 10% which the literature suggests should enhance flight. Flying ability was maintained regardless of treatment. Examining individual variation revealed the same precise patterns as in the first experiment. We conclude that prey may alter their mass and evasive actions in response to predation risk, but their escape ability remains robust and inelastic, presumably because disabling oneself is likely to lead to disastrous consequences. We suggest that animals may only face a mass-dependent predation risk trade-off in a narrow set of circumstances linked to life-history stages that require large amounts of mass gain, for example, parturition and migration. A lay summary is available for this article

Astronomical and Tectonic Influences on Climate and Deposition Revealed Through Radioisotopic Geochronology and Bayesian Age-Depth Modeling of the Early Eocene Green River Formation, Wyoming, USA

The Wilkins Peak Member (WPM) of the Green River Formation in Wyoming, USA, comprises alternating lacustrine and alluvial strata that preserve a record of terrestrial climate during the early Eocene climatic optimum. We use a Bayesian framework to develop age-depth models for three sites, based on new 40Ar/39Ar sanidine and 206Pb/238U zircon ages from seven tuffs. The new models provide two- to ten-fold increases in temporal resolution compared to previous radioisotopic age models, confirming eccentricity-scale pacing of WPM facies, and permitting their direct comparison to astronomical solutions. Starting at ca. 51 Ma, the median ages for basin-wide flooding surfaces atop six successive alluvial marker beds coincide with short eccentricity maxima in the astronomical solutions. These eccentricity maxima have been associated with hyperthermal events recorded in marine strata during the early Eocene. WPM strata older than ca. 51 Ma do not exhibit a clear relationship to the eccentricity solutions, but accumulated 31%–35% more rapidly, suggesting that the influence of astronomical forcing on sedimentation was modulated by basin tectonics. Additional high-precision radioisotopic ages are needed to reduce the uncertainty of the Bayesian model, but this approach shows promise for unambiguous evaluation of the phase relationship between alluvial marker beds and theoretical eccentricity solutions

Engagement in the Data Collection Phase of the Scientific Process is Key for Enhancing Learning Gains

Most programs that create opportunities for the public to engage in scientific research invite the public to collect data, but there is a call to expand opportunities for engagement in additional aspects of the scientific process. One reason behind this call is the hypothesis that people who participate to a greater degree in the scientific process experience more robust learning outcomes. To test this hypothesis, we conducted a quasi-experiment by using a pre-post survey design and comparing varying degrees of participation in a Bird Cams Lab investigation. Bird Cams Lab was a virtual space in which the public worked with scientists to design and implement co-created investigations involving live streaming or recorded footage of birds. We found that the higher the degree of participation in the investigation, the greater the increase in content knowledge, self-efficacy, and self-reported improvement in science inquiry skills. Interestingly, involvement in data collection was associated with the greatest gains in content knowledge and self-efficacy regardless of involvement in other parts of the scientific process. For programs with limited funding and resources that seek to increase participants’ content knowledge and self-efficacy, focusing efforts on supporting data collection may be the most impactful

Atrial fibrillation genetic risk differentiates cardioembolic stroke from other stroke subtypes

Objective: We sought to assess whether genetic risk factors for atrial fibrillation (AF) can explain cardioembolic stroke risk. Methods: We evaluated genetic correlations between a previous genetic study of AF and AF in the presence of cardioembolic stroke using genome-wide genotypes from the Stroke Genetics Network (N = 3,190 AF cases, 3,000 cardioembolic stroke cases, and 28,026 referents). We tested whether a previously validated AF polygenic risk score (PRS) associated with cardioembolic and other stroke subtypes after accounting for AF clinical risk factors. Results: We observed a strong correlation between previously reported genetic risk for AF, AF in the presence of stroke, and cardioembolic stroke (Pearson r = 0.77 and 0.76, respectively, across SNPs with p < 4.4 × 10−4 in the previous AF meta-analysis). An AF PRS, adjusted for clinical AF risk factors, was associated with cardioembolic stroke (odds ratio [OR] per SD = 1.40, p = 1.45 × 10−48), explaining ∼20% of the heritable component of cardioembolic stroke risk. The AF PRS was also associated with stroke of undetermined cause (OR per SD = 1.07, p = 0.004), but no other primary stroke subtypes (all p > 0.1). Conclusions: Genetic risk of AF is associated with cardioembolic stroke, independent of clinical risk factors. Studies are warranted to determine whether AF genetic risk can serve as a biomarker for strokes caused by AF

The Medicine Tree: Unsettling palaeoecological perceptions of past environments and human activity

In this paper, we consider palaeoecological approaches to past landscapes and reflect upon how these are relevant to archaeological themes concerning concepts of environmental change and the role of past and present human communities in these processes. In particular, we highlight the importance of local context in the perception and understanding of landscape. Utilising a case study from Nepal, we look to ‘unsettle’ a conventional palaeoecological interpretation of a pollen record, originally constructed on western ecological principles, and instead draw on an interpretative perspective rooted in local Buddhist ecological knowledge, or a ‘folk taxonomy’, known as ‘The Medicine Tree’. We discuss how the interpretations of patterns and processes of vegetation change from a pollen record are not necessarily absolute. In particular, we outline how the palaeoecological frame of enquiry and reference is rooted in an essentially Eurocentric, Western scientific paradigm, which, in turn, shapes how we perceive and conceive of past landscapes and the role of ‘anthropogenic impact’ on vegetation. The aim of this is not to suggest that scientific approaches to the ‘reconstruction’ of past landscapes are necessarily invalid, but to illustrate how ‘empirical’ scientific methods and interpretations in archaeological science are contingent upon specific social and cultural frames of reference. We discuss the broader relevance of this, such as how we interpret past human activity and perception of landscape change, the ways in which we might look to mobilise research in the context of contemporary problems, issues concerning ‘degraded landscapes’ and how we incorporate local and archaeological perspectives with palaeoecology within an interconnected and iterative process

The type II poly(A)-binding protein PABP-2 genetically interacts with the let-7 miRNA and elicits heterochronic phenotypes in Caenorhabditis elegans

The type II poly(A)-binding protein PABP2/PABPN1 functions in general mRNA metabolism by promoting poly(A) tail formation in mammals and flies. It also participates in poly(A) tail shortening of specific mRNAs in flies, and snoRNA biogenesis in yeast. We have identified Caenorhabditis elegans pabp-2 as a genetic interaction partner of the let-7 miRNA, a widely conserved regulator of animal stem cell fates. Depletion of PABP-2 by RNAi suppresses loss of let-7 activity, and, in let-7 wild-type animals, leads to precocious differentiation of seam cells. This is not due to an effect on let-7 biogenesis and activity, which remain unaltered. Rather, PABP-2 levels are developmentally regulated in a let-7-dependent manner. Moreover, using RNAi PABP-2 can be depleted by >80% without significantly impairing larval viability, mRNA levels or global translation. Thus, it unexpectedly appears that the bulk of PABP-2 is dispensable for general mRNA metabolism in the larva and may instead have more restricted, developmental functions. This observation may be relevant to our understanding of why the phenotypes associated with human PABP2 mutation in oculopharyngeal muscular dystrophy (OPMD) seem to selectively affect only muscle cells

New genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk.

Levels of circulating glucose are tightly regulated. To identify new loci influencing glycemic traits, we performed meta-analyses of 21 genome-wide association studies informative for fasting glucose, fasting insulin and indices of beta-cell function (HOMA-B) and insulin resistance (HOMA-IR) in up to 46,186 nondiabetic participants. Follow-up of 25 loci in up to 76,558 additional subjects identified 16 loci associated with fasting glucose and HOMA-B and two loci associated with fasting insulin and HOMA-IR. These include nine loci newly associated with fasting glucose (in or near ADCY5, MADD, ADRA2A, CRY2, FADS1, GLIS3, SLC2A2, PROX1 and C2CD4B) and one influencing fasting insulin and HOMA-IR (near IGF1). We also demonstrated association of ADCY5, PROX1, GCK, GCKR and DGKB-TMEM195 with type 2 diabetes. Within these loci, likely biological candidate genes influence signal transduction, cell proliferation, development, glucose-sensing and circadian regulation. Our results demonstrate that genetic studies of glycemic traits can identify type 2 diabetes risk loci, as well as loci containing gene variants that are associated with a modest elevation in glucose levels but are not associated with overt diabetes

Virulence Regulator EspR of Mycobacterium tuberculosis Is a Nucleoid-Associated Protein

The principal virulence determinant of Mycobacterium tuberculosis (Mtb), the ESX-1 protein secretion system, is positively controlled at the transcriptional level by EspR. Depletion of EspR reportedly affects a small number of genes, both positively or negatively, including a key ESX-1 component, the espACD operon. EspR is also thought to be an ESX-1 substrate. Using EspR-specific antibodies in ChIP-Seq experiments (chromatin immunoprecipitation followed by ultra-high throughput DNA sequencing) we show that EspR binds to at least 165 loci on the Mtb genome. Included in the EspR regulon are genes encoding not only EspA, but also EspR itself, the ESX-2 and ESX-5 systems, a host of diverse cell wall functions, such as production of the complex lipid PDIM (phenolthiocerol dimycocerosate) and the PE/PPE cell-surface proteins. EspR binding sites are not restricted to promoter regions and can be clustered. This suggests that rather than functioning as a classical regulatory protein EspR acts globally as a nucleoid-associated protein capable of long-range interactions consistent with a recently established structural model. EspR expression was shown to be growth phase-dependent, peaking in the stationary phase. Overexpression in Mtb strain H37Rv revealed that EspR influences target gene expression both positively or negatively leading to growth arrest. At no stage was EspR secreted into the culture filtrate. Thus, rather than serving as a specific activator of a virulence locus, EspR is a novel nucleoid-associated protein, with both architectural and regulatory roles, that impacts cell wall functions and pathogenesis through multiple genes