Biology subjects

Moltchanova, E.

Publications and source records attributed to Moltchanova, E..

3 recordsLinked to original sources

bioRxiv2021

Disentangling niche theory and beta diversity change

Beta diversity describes the differences in species composition among communities. Changes in beta diversity over time are thought to be due to selection based on species niche characteristics. For example, theory predicts that selection that favours habitat specialists will increase beta diversity. In practice, ecologists struggle to predict how beta diversity changes. To remedy this problem, we propose a novel solution that formally measures selections effects on beta diversity. Using the Price equation, we show how change in beta diversity over time can be partitioned into fundamental mechanisms including selection among species, variable selection among communities, drift, and immigration. A key finding of our approach is that a species short-term impact on beta diversity cannot be predicted using information on its long-term environmental requirements (i.e. its niche). We illustrate how our approach can be used to partition causes of diversity change in a montane tropical forest before and after an intense hurricane. Previous work in this system highlighted the resistance of habitat specialists and the recruitment of light-demanding species but was unable to quantify the importance of these effects on beta diversity. Using our approach, we show that changes in beta diversity were consistent with ecological drift. We use these results to highlight the opportunities presented by a synthesis of beta diversity and formal models of selection.

ecology↗

bioRxiv2020

Modeling Risks and Mitigation Options for the Chronic Wasting Disease (CWD) in Scandinavia

Chronic wasting disease (CWD) is a contagious neural prion-disease affecting deer populations in North America with severe ecological and societal consequences. CWD is fatal and infectious prions spread and remain in the environment for many years even without animals present. The recent appearance of CWD in reindeers in Norway called for a drastic culling operation to prevent further spreading of the disease. This appears to have stopped the spreading of CWD among reindeers, but due to the persistence of CWD prions in the environment a reappearance of new cases among reindeer or other species in the future cannot be excluded. To evaluate the risks and the effectiveness of alternative management (monitoring and culling) options, we developed a model of CWD dynamics and management. The model includes stochastic population and spatial dynamics of the four relevant deer species in northern Sweden and Norway: reindeer (Rangifer tarandus), roe deer (Capreolus capreolus), red deer (Cervus elaphus) and moose (Alces alces). Transmission of CWD is modelled via direct contacts and via the environment. The model was parameterized and calibrated based on CWD studies from USA, data from the Norwegian CWD cases, and local deer population and vegetation data. The results indicate that without management, a CWD epidemic can be initiated by a single infected reindeer and would spread to other deer species. It would lead to dramatic population declines of reindeer and red deer and would also reduce the populations of roe deer and moose. The disease prevalence would stabilise at a about 50% after 50 years, as observed in some areas in the USA. A management strategy to cull only visibly sick animals, even with very efficient detection, cannot prevent a catastrophic development but merely slow the outbreak. To prevent an outbreak and the establishment of CWD it is necessary to cull all individuals, not only visibly sick ones, of an affected species in a relatively large area (30x30 km in our model) once a case is detected. Further, to prevent a slow buildup of CWD in the environment and eliminate the risk of outbreaks in the future it is necessary to expand this area of culling even further. Although the model has not yet been thoroughly validated due to scarcity of data, the results suggest that the drastic culling done in Norway was appropriate and necessary to prevent establishment of CWD and that further monitoring and potential culling is required to prevent outbreaks in the future.

ecology↗

bioRxiv2017

Genetic architecture of early childhood growth phenotypes gives insights into their link with later obesity

Early childhood growth patterns are associated with adult metabolic health, but the underlying mechanisms are unclear. We performed genome-wide meta-analyses and follow-up in up to 22,769 European children for six early growth phenotypes derived from longitudinal data: peak height and weight velocities, age and body mass index (BMI) at adiposity peak (AP ~9 months) and rebound (AR ~5-6 years). We identified four associated loci (P< 5x10-8): LEPR/LEPROT with BMI at AP, FTO and TFAP2B with Age at AR and GNPDA2 with BMI at AR. The observed AR-associated SNPs at FTO, TFAP2B and GNPDA2 represent known adult BMI-associated variants. The common BMI at AP associated variant at LEPR/LEPROT was not associated with adult BMI but was associated with LEPROT gene expression levels, especially in subcutaneous fat (P<2x10-51). We identify strong positive genetic correlations between early growth and later adiposity traits, and analysis of the full discovery stage results for Age at AR revealed enrichment for insulin-like growth factor 1 (IGF-1) signaling and apolipoprotein pathways. This genome-wide association study suggests mechanistic links between early childhood growth and adiposity in later childhood and adulthood, highlighting these early growth phenotypes as potential targets for the prevention of obesity.

genomics↗