scholarly journals Recent immigrants alter the quantitative genetic architecture of paternity in song sparrows

2020 ◽  
Vol 4 (2) ◽  
pp. 124-136
Author(s):  
Jane M. Reid ◽  
Peter Arcese
Heredity ◽  
2009 ◽  
Vol 104 (1) ◽  
pp. 20-27 ◽  
Author(s):  
H Kuukka-Anttila ◽  
N Peuhkuri ◽  
I Kolari ◽  
T Paananen ◽  
A Kause

2020 ◽  
Vol 287 (1928) ◽  
pp. 20200057
Author(s):  
Allison Jaffe ◽  
Madeline P. Burns ◽  
Julia B. Saltz

Social interactions can influence the expression and underlying genetic basis of many traits. Yet, empirical investigations of indirect genetic effects (IGEs) and genotype-by-genotype epistasis—quantitative genetics parameters representing the role of genetic variation in a focal individual and its interacting partners in producing the observed trait values—are still scarce. While it is commonly observed that an individual's traits are influenced by the traits of interacting conspecifics, representing social plasticity, studying this social plasticity and its quantitative-genetic basis is notoriously challenging. These challenges are compounded when individuals interact in groups, rather than (simpler) dyads. Here, we investigate the genetic architecture of social plasticity for exploratory behaviour, one of the most intensively studied behaviours in recent decades. Using genotypes of Drosophila simulans , we measured genotypes both alone, and in social groups representing a mix of two genotypes. We found that females adjusted their exploratory behaviour based on the behaviour of others in the group, representing social plasticity. However, the direction of this plasticity depended on the identity of group members: focal individuals were more likely to emerge from a refuge if group members who were the same genotype as the focal remained inside for longer. By contrast, focal individuals were less likely to emerge from a refuge if partner-genotype group members remained inside for longer. Exploratory behaviour also depended on the identities of both genotypes that composed the group. Together, these findings demonstrate genotype-by-genotype epistasis for exploratory behaviour both within and among groups.


PLoS ONE ◽  
2013 ◽  
Vol 8 (7) ◽  
pp. e68828 ◽  
Author(s):  
Mary E. Oswald ◽  
Mathew Singer ◽  
Barrie D. Robison

2009 ◽  
Vol 32 (3-4) ◽  
pp. 282-283
Author(s):  
Bart Kempenaers ◽  
Wolfgang Forstmeier

AbstractQuantitative genetic studies of human aggressive behavior only partly support the claim of social role theory that individual differences in aggressive behavior are learnt rather than innate. As to its heritable component, future studies on the genetic architecture of aggressive behavior across different contexts could shed more light on the evolutionary origins of male-female versus male-male aggression.


2021 ◽  
Author(s):  
Antoine Fraimout ◽  
Zitong Li ◽  
Mikko J. Sillanpää ◽  
Pasi Rastas ◽  
Juha Merilä

ABSTRACTAdditive and dominance genetic variances underlying the expression of quantitative traits are important quantities for predicting short-term responses to selection, but they are notoriously challenging to estimate in most wild animal populations. Using estimates of genome-wide identity-by-descent (IBD) sharing from autosomal SNP loci, we estimated quantitative genetic parameters for traits known to be under directional natural selection in nine-spined sticklebacks (Pungitius pungitius) and compared these to traditional pedigree-based estimators. Using four different datasets, with varying sample sizes and pedigree complexity, we further assessed the performance of different Genomic Relationship Matrices (GRM) to estimate additive and dominance variance components. Large variance in IBD relationships allowed accurate estimation of genetic variance components, and revealed significant heritability for all measured traits, with negligible dominance contributions. Genome-partitioning analyses revealed that all traits have a polygenic basis and are controlled by genes at multiple chromosomes. The results demonstrate how large full-sib families of highly fecund vertebrates can be used to obtain accurate estimates quantitative genetic parameters to provide insights on genetic architecture of quantitative traits in non-model organisms from the wild. This approach should be particularly useful for studies requiring estimates of genetic variance components from multiple populations as for instance when aiming to infer the role of natural selection as a cause for population differentiation in quantitative traits.


2005 ◽  
Vol 7 (2) ◽  
pp. 125-135 ◽  

Specifying the complex genetic architecture of the "fuzzy" clinical phenotype of schizophrenia is an imposing problem. Utilizing metabolic, neurocognitive, and neurophysiological "intermediate" endophenotypic measures offers significant advantages from a statistical genetics standpoint. Endophenotypic measures are amenable to quantitative genetic analyses, conferring upon them a major methodological advantage compared with largely qualitative diagnoses using the Diagnostic and Statistical Manual of Mental Health, 4th Edition (DSM-IV). Endophenotypic deficits occur across the schizophrenia spectrum in schizophrenia patients, schizotypal patients, and clinically unaffected relatives of schizophrenia patients. Neurophysiological measures, such as P50 event-related suppression and the prepulse inhibition (PPI) of the startle response, are endophenotypes that can be conceptualized as being impaired because of a single genetic abnormality in the functional cascade of DNA to RNA to protein. The "endophenotype approach" is also being used to understand other medical disorders, such as colon cancer, hemochromatosis, and hypertension, where there is interplay between genetically conferred vulnerability and nongenetic stressors. The power and utility of utilizing endophenotypes to understand the genetics of schizophrenia is discussed in detail in this article.


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