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Population genetic consequences of the Allee effect and the role of offspring-number variation.

ABSTRACT: A strong demographic Allee effect in which the expected population growth rate is negative below a certain critical population size can cause high extinction probabilities in small introduced populations. But many species are repeatedly introduced to the same location and eventually one population may overcome the Allee effect by chance. With the help of stochastic models, we investigate how much genetic diversity such successful populations harbor on average and how this depends on offspring-number variation, an important source of stochastic variability in population size. We find that with increasing variability, the Allee effect increasingly promotes genetic diversity in successful populations. Successful Allee-effect populations with highly variable population dynamics escape rapidly from the region of small population sizes and do not linger around the critical population size. Therefore, they are exposed to relatively little genetic drift. It is also conceivable, however, that an Allee effect itself leads to an increase in offspring-number variation. In this case, successful populations with an Allee effect can exhibit less genetic diversity despite growing faster at small population sizes. Unlike in many classical population genetics models, the role of offspring-number variation for the population genetic consequences of the Allee effect cannot be accounted for by an effective-population-size correction. Thus, our results highlight the importance of detailed biological knowledge, in this case on the probability distribution of family sizes, when predicting the evolutionary potential of newly founded populations or when using genetic data to reconstruct their demographic history.

SUBMITTER: Wittmann MJ

PROVIDER: S-EPMC4174943 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:The offspring of older fathers have an increased risk of neurodevelopmental disorders such as schizophrenia and autism. It has been proposed that de novo point mutations and copy number variants (CNVs) in the continually dividing spermatogonia underlie this association. In light of the evidence implicating CNVs with schizophrenia and autism, here we use a mouse model to test the hypothesis that the offspring of older males have an increased risk of de novo CNVs. Three-month-old and fourteen- to sixteen-month-old C57BL/6J sires were mated with three-month-old dams to create control offspring and offspring of old sires, respectively. Applying genome-wide microarray screening technology, seven distinct CNVs were identified in a discovery set of twelve offspring and their parents. Competitive quantitative PCR was employed to confirm the variants and establish their frequency in a replication set of 77 offspring and their parents. Six de novo CNVs were detected in the offspring of older sires, while none were detected in the control group. One of the de novo CNVs involved Auts2 (autism susceptibility candidate 2), and other CNVs included genes linked to schizophrenia, autism and brain development. Two of the CNVs were associated with behavioural and/or neuroanatomical phenotypic features. This is the first experimental demonstration that the offspring of older males have more de novo CNVs. The results suggest that offspring of older fathers may be at increased risk of neurodevelopmental disorders such as schizophrenia and autism via the generation of de novo CNV in the male germline. In light of the trends for delayed parenthood in many societies, and in light of the potential for these CNVs to accumulate over subsequent generations, the impact of these mechanisms on the health of future generations warrants closer scrutiny. 2 sires of advanced paternal age (12-16 months of age) and 2 control (3 months of age) sires were mated to dams (3 months of age) to create 6 offspring of advanced paternal age (APA) and 6 control offspring (C), respectively, with an even number of sexes within each group of offspring. A commerical aCGH and a custom CNV array (both supplied by Agilent) were used in combination to detect copy number variations in the genomes of the offspring and their parents. DNA from all male animals was hybridized against a male reference animal and that from all female animals against a female reference animal.

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Population genetic consequences of the Allee effect and the role of offspring-number variation.

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