scholarly journals Linking genetic merit to sparse behavioral data: behavior and genetic effects on lamb growth in Soay sheep

2019 ◽  
Author(s):  
Charlotte E Regan ◽  
Josephine M Pemberton ◽  
Jill G Pilkington ◽  
Per T Smiseth ◽  
Alastair J Wilson
Keyword(s):  
Genetic Variation ◽  
Parental Care ◽  
Natural Populations ◽  
Genetic Effects ◽  
Breeding Value ◽  
Offspring Performance ◽  
Genetic Studies ◽  
Soay Sheep ◽  
Lamb Growth

Abstract Wild quantitative genetic studies have focused on a subset of traits (largely morphological and life history), with others, such as behaviors, receiving much less attention. This is because it is challenging to obtain sufficient data, particularly for behaviors involving interactions between individuals. Here, we explore an indirect approach for pilot investigations of the role of genetic differences in generating variation in parental care. Variation in parental genetic effects for offspring performance is expected to arise from among-parent genetic variation in parental care. Therefore, we used the animal model to predict maternal breeding values for lamb growth and used these predictions to select females for field observation, where maternal and lamb behaviors were recorded. Higher predicted maternal breeding value for lamb growth was associated with greater suckling success, but not with any other measures of suckling behavior. Though our work cannot explicitly estimate the genetic basis of the specific traits involved, it does provide a strategy for hypothesis generation and refinement that we hope could be used to justify data collection costs needed for confirmatory studies. Here, results suggest that behavioral genetic variation is involved in generating maternal genetic effects on lamb growth in Soay sheep. Though important caveats and cautions apply, our approach may extend the ability to initiate more genetic investigations of difficult-to-study behaviors and social interactions in natural populations.

scholarly journals Reexamining Waddington: Canalization and new mutations are not required for the evolution of genetic assimilation

2022 ◽  
Author(s):  
Sarah Ruth Marzec ◽  
Katharine Pelletier ◽  
Amy Hui-Pin Chang ◽  
Ian Dworkin
Keyword(s):  
Genetic Variation ◽  
Natural Populations ◽  
Genetic Assimilation ◽  
Wing Morphology ◽  
Relative Contribution ◽  
Fitness Consequences ◽  
Selection Experiments ◽  
Environmentally Sensitive ◽  
New Mutations

Over 65 years ago, Waddington demonstrated ancestrally phenotypically plastic traits can evolve to become constitutive, a process he termed genetic assimilation. Genetic assimilation evolves rapidly, assumed to be in large part due to segregating genetic variation only expressed in rare/novel environments, but otherwise phenotypically cryptic. Despite previous work suggesting a substantial role of cryptic genetic variation contributing to the evolution of genetic assimilation, some have argued for a prominent role for new mutations of large effect concurrent with selection. Interestingly, Waddington was less concerned by the relative contribution of CGV or new variants, but aimed to test the role of canalization, an evolved form of robustness. While canalization has been extensively studied, its role in the evolution of genetic assimilation is disputed, in part because explicit tests of evolved robustness are lacking. To address these questions, we recreated Waddington's selection experiments on an environmentally sensitive change in Drosophila wing morphology (crossvein development), using many independently evolved replicate lineages. Using these, we show that 1) a polygenic CGV, but not new variants of large effect are largely responsible for the evolved response demonstrated using both genomic and genetic approaches. 2) Using both environmental manipulations and mutagenesis of the evolved lineages that there is no evidence for evolved changes in canalization contributing to genetic assimilation. Finally, we demonstrate that 3) CGV has potentially pleiotropic and fitness consequences in natural populations and may not be entirely cryptic.

The Heritability of Attachment Systems

2020 ◽  
Author(s):  
Nicole Barbaro
Keyword(s):  
Genetic Variation ◽  
Attachment Theory ◽  
Critical Evaluation ◽  
Twin Studies ◽  
Behavior Genetic ◽  
Genetic Studies ◽  
Additive Genetic Effects ◽  
Published Research ◽  
Broad Consensus

Attachment theory has strong environmental origins, from which it has been the broad consensus that variation in attachment is caused by variation in environments (shared and non-shared), with little role of genetic variation, especially in infants. However, the state of the behavior genetic evidence needs critical evaluation to discern whether such environmentalist claims are warranted. Here, I demonstrate that the majority of the available twin studies are not adequately powered to detect additive genetic effects if present, and that the majority of twin studies in infants are not adequately powered to detect shared environmental effects. Within the published research, I can find only three adequately powered twin studies on attachment: one in infants, one in adolescents, and one in adults. I conclude by presenting five observations from behavior genetic studies that future developmental frameworks of attachment must account for.

scholarly journals The quantitative genetics of the prevalence of infectious diseases: hidden genetic variation due to Indirect Genetic Effects dominates heritable variation and response to selection

Genetics ◽  
2021 ◽  
Author(s):  
Piter Bijma ◽  
Andries D Hulst ◽  
Mart C M de Jong
Keyword(s):  
Genetic Variation ◽  
Infectious Diseases ◽  
Quantitative Genetics ◽  
Disease Status ◽  
Genetic Effects ◽  
Breeding Value ◽  
Response To Selection ◽  
Heritable Variation ◽  
Genetic Theory ◽  
Quantitative Genetic

Abstract Infectious diseases have profound effects on life, both in nature and agriculture. However, a quantitative genetic theory of the host population for the endemic prevalence of infectious diseases is almost entirely lacking. While several studies have demonstrated the relevance of transmission of infections for heritable variation and response to selection, current quantitative genetics ignores transmission. Thus, we lack concepts of breeding value and heritable variation for endemic prevalence, and poorly understand response of endemic prevalence to selection. Here we integrate quantitative genetics and epidemiology, and propose a quantitative genetic theory for the basic reproduction number R0 and for the endemic prevalence of an infection. We first identify the genetic factors that determine the prevalence. Subsequently we investigate the population level consequences of individual genetic variation, for both R0 and the endemic prevalence. Next, we present expressions for the breeding value and heritable variation, for endemic prevalence and individual binary disease status, and show that these depend strongly on the prevalence. Results show that heritable variation for endemic prevalence is substantially greater than currently believed, and increases strongly when prevalence decreases, while heritability of disease status approaches zero. As a consequence, response of the endemic prevalence to selection for lower disease status accelerates considerably when prevalence decreases, in contrast to classical predictions. Finally, we show that most heritable variation for the endemic prevalence is hidden in indirect genetic effects, suggesting a key role for kin-group selection in the evolutionary history of current populations and for genetic improvement in animals and plants.

Genetic background of cholesterol absorption efficacy. The role of Niemann–Pick C1-like 1 receptor and its genetic variation in lipid metabolism

2010 ◽  
Vol 151 (34) ◽  
pp. 1376-1383 ◽  
Author(s):  
Mariann Harangi ◽  
István Balogh ◽  
János Harangi ◽  
György Paragh
Keyword(s):  
Genetic Variation ◽  
Lipid Metabolism ◽  
Genetic Background ◽  
Cholesterol Absorption ◽  
Niemann Pick

A Niemann–Pick C1-like-1 egy szterolfelismerő domént tartalmazó membránfehérje, amelyet nagy számban expresszálnak csúcsi felszínükön a bélhámsejtek. Az utóbbi évek vizsgálatai azt igazolták, hogy ez a fehérje szükséges a szabad koleszterin bejutásához a bélhámsejtekbe a bél lumenéből. Biokémiai vizsgálatok azt igazolták, hogy a Niemann–Pick C1-like-1-hez kötődik az ezetimib, amely egy hatékony koleszterinfelszívódást gátló szer. A bélből történő koleszterinfelszívódás ütemében és az ezetimibkezelés hatékonyságában tapasztalt egyéni eltérések hátterében felmerült néhány Niemann–Pick C1-like-1 génvariáció oki szerepe.

The role of hormones

2018 ◽  
Author(s):  
H. Frederik Nijhout ◽  
Emily Laub
Keyword(s):  
Phenotypic Plasticity ◽  
Social Behavior ◽  
Parental Care ◽  
Juvenile Hormone ◽  
Reproductive Behavior ◽  
Hormonal Control ◽  
Plastic Trait

Many behaviors of insects are stimulated, modified, or modulated by hormones. The principal hormones involved are the same as the ones that control moulting, metamorphosis, and other aspects of development, principally ecdysone and juvenile hormone. In addition, a small handful of neurosecretory hormones are involved in the control of specific behaviors. Because behavior is a plastic trait, this chapter begins by outlining the biology and hormonal control of phenotypic plasticity in insects, and how the hormonal control of behavior fits in with other aspects of the control of phenotypic plasticity. The rest of the chapter is organized around the diversity of behaviors that are known to be controlled by or affected by hormones. These include eclosion and moulting behavior, the synthesis and release of pheromones, migration, parental care, dominance, reproductive behavior, and social behavior.

scholarly journals Uric Acid and Hypertension: Prognostic Role and Guide for Treatment

2021 ◽  
Vol 10 (3) ◽  
pp. 448
Author(s):  
Federica Piani ◽  
Arrigo F. G. Cicero ◽  
Claudio Borghi
Keyword(s):  
Clinical Trials ◽  
Uric Acid ◽  
Mendelian Randomization ◽  
Strong Association ◽  
Epidemiological Studies ◽  
Hypertensive Disease ◽  
Genetic Studies ◽  
Lowering Therapy ◽  
The Relationship

The relationship between serum uric acid (SUA) and hypertension has been a subject of increasing interest since the 1870 discovery by Frederick Akbar Mahomed. Several epidemiological studies have shown a strong association between high SUA levels and the presence or the development of hypertension. Genetic analyses have found that xanthine oxidoreductase (XOR) genetic polymorphisms are associated with hypertension. However, genetic studies on urate transporters and Mendelian randomization studies failed to demonstrate a causal relationship between SUA and hypertension. Results from clinical trials on the role of urate-lowering therapy in the management of patients with hypertension are not uniform. Our study sought to analyze the prognostic and therapeutic role of SUA in the hypertensive disease, from uric acid (UA) biology to clinical trials on urate-lowering therapies.

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