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Most animals live in seasonal environments and experience very different conditions throughout the year. Behavioral strategies like migration, hibernation, and a life cycle adapted to the local seasonality help to cope with fluctuations in environmental conditions. Thus, how an individual utilizes the environment depends both on the current availability of habitat and the behavioral prerequisites of the individual at that time. While the increasing availability and richness of animal movement data has facilitated the development of algorithms that classify behavior by movement geometry, changes in the environmental correlates of animal movement have so far not been exploited for a behavioral annotation. Here, we suggest a method that uses these changes in individual–environment associations to divide animal location data into segments of higher ecological coherence, which we term niche segmentation. We use time series of random forest models to evaluate the transferability of habitat use over time to cluster observational data accordingly. We show that our method is able to identify relevant changes in habitat use corresponding to both changes in the availability of habitat and how it was used using simulated data, and apply our method to a tracking data set of common teal (Anas crecca). The niche segmentation proved to be robust, and segmented habitat suitability outperformed models neglecting the temporal dynamics of habitat use. Overall, we show that it is possible to classify animal trajectories based on changes of habitat use similar to geometric segmentation algorithms. We conclude that such an environmentally informed classification of animal trajectories can provide new insights into an individuals' behavior and enables us to make sensible predictions of how suitable areas might be connected by movement in space and time.
Fanconi anemia (FA) is a genetically heterogeneous disorder with 22 disease-causing genes reported to date. In some FA genes, monoallelic mutations have been found to be associated with breast cancer risk, while the risk associations of others remain unknown. The gene for FA type C, FANCC, has been proposed as a breast cancer susceptibility gene based on epidemiological and sequencing studies. We used the Oncoarray project to genotype two truncating FANCC variants (p.R185X and p.R548X) in 64,760 breast cancer cases and 49,793 controls of European descent. FANCC mutations were observed in 25 cases (14 with p.R185X, 11 with p.R548X) and 26 controls (18 with p.R185X, 8 with p.R548X). There was no evidence of an association with the risk of breast cancer, neither overall (odds ratio 0.77, 95%CI 0.44–1.33, p = 0.4) nor by histology, hormone receptor status, age or family history. We conclude that the breast cancer risk association of these two FANCC variants, if any, is much smaller than for BRCA1, BRCA2 or PALB2 mutations. If this applies to all truncating variants in FANCC it would suggest there are differences between FA genes in their roles on breast cancer risk and demonstrates the merit of large consortia for clarifying risk associations of rare variants.