Despite numerous studies examining the fitness consequences of animal personalities, predictions concerning the relationship between personality and survival are not consistent with empirical observations. Theory predicts that individuals who are risky (i.e. bold, active and aggressive) should have higher rates of mortality; however, empirical evidence shows high levels of variation in behaviour–survival relationships in wild populations. We suggest that this mismatch between predictions under theory and empirical observations results from environmental contingencies that drive heterogeneity in selection. This uncertainty may constrain any universal directional relationships between personality traits and survival. Specifically, we hypothesize that spatiotemporal fluctuations in perceived risk that arise from variability in refuge abundance and competitor density alter the relationship between personality traits and survival. In a large‐scale manipulative experiment, we trapped four small mammal species in five subsequent years across six forest stands treated with different management practices in Maine, United States. Stands all occur within the same experimental forest but contain varying amounts of refuge and small mammal densities fluctuate over time and space. We quantified the effects of habitat structure and competitor density on the relationship between personality traits and survival to assess whether directional relationships differed depending on environmental contingencies. In the two most abundant species, deer mice and southern red‐backed voles, risky behaviours (i.e. higher aggression and boldness) predicted apparent monthly survival probability. Mice that were more aggressive (less docile) had higher survival. Voles that were bolder (less timid) had higher survival, but in the risky forest stands only. Additionally, traits associated with stress coping and de‐arousal increased survival probability in both species at high small mammal density but decreased survival at low density. In the two less abundant study species, there was no evidence for an effect of personality traits on survival. Our field experiment provides partial support for our hypothesis: that spatiotemporal fluctuations in refuge abundance and competitor density alter the relationship between personality traits and survival. Our findings also suggest that behaviours associated with stress coping and de‐arousal may be subject to density‐dependent selection and should be further assessed and incorporated into theory.
Ecological and environmental factors can influence the transmission of infectious diseases. They can accomplish this via effects on host susceptibility and exposure to infection, which are governed by host physiology and behavior, respectively. To better inform disease control, more information is needed about how extrinsic factors affect physiological and behavioral processes that determine transmission. We investigated how heterospecific competitors and seasonality may influence host susceptibility and intraspecific contact rates using a directly transmitted disease system, the North American deer mouse (
- Award ID(s):
- 1836793
- NSF-PAR ID:
- 10359934
- Publisher / Repository:
- Wiley Blackwell (John Wiley & Sons)
- Date Published:
- Journal Name:
- Ecosphere
- Volume:
- 12
- Issue:
- 6
- ISSN:
- 2150-8925
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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Abstract Predators may create healthier prey populations by selectively removing diseased individuals. Predators typically prefer some ages of prey over others, which may, or may not, align with those prey ages that are most likely to be diseased.
The interaction of age‐specific infection and predation has not been previously explored and likely has sizable effects on disease dynamics. We hypothesize that predator cleansing effects will be greater when the disease and predation occur in the same prey age groups.
We examine the predator cleansing effect using a model where both vulnerability to predators and pathogen prevalence vary with age. We tailor this model to chronic wasting disease (CWD) in mule deer and elk populations in the Greater Yellowstone Ecosystem, with empirical data from Yellowstone grey wolves and cougars.
Model results suggest that under moderate, yet realistic, predation pressure from cougars and wolves independently, predators may decrease CWD outbreak size substantially and delay the accumulation of symptomatic deer and elk. The magnitude of this effect is driven by the ability of predators to selectively remove late‐stage CWD infections that are likely the most responsible for transmission, but this may not be the age class they typically select. Thus, predators that select for infected young adults over uninfected juveniles have a stronger cleansing effect, and these effects are strengthened when transmission rates increase with increasing prey morbidity. There are also trade‐offs from a management perspective—that is, increasing predator kill rates can result in opposing forces on prey abundance and CWD prevalence.
Our modelling exploration shows that predators have the potential to reduce prevalence in prey populations when prey age and disease severity are considered, yet the strength of this effect is influenced by predators' selection for demography or body condition. Current CWD management focuses on increasing cervid hunting as the primary management tool, and our results suggest predators may also be a useful tool under certain conditions, but not necessarily without additional impacts on host abundance and demography. Protected areas with predator populations will play a large role in informing the debate over predator impacts on disease.
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We examined high‐altitude deer mice, which have evolved a high capacity for aerobic thermogenesis, to determine the mechanisms of mitochondrial plasticity during chronic exposure to cold and hypoxia, alone and in combination.
Cold exposure in normoxia or hypoxia increased mitochondrial leak respiration and decreased phosphorylation efficiency and OXPHOS coupling efficiency, which may serve to augment non‐shivering thermogenesis. Cold also increased muscle oxidative capacity, but reduced the capacity for mitochondrial respiration via complex II relative to complexes I and II combined.
High‐altitude mice had a more oxidative muscle phenotype than low‐altitude mice.
Therefore, both plasticity and evolved changes in muscle mitochondria contribute to thermogenesis at high altitude.
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