Selective Breeding to Support the Long-Term Persistence of Coral Reefs

2021 ◽  
Author(s):  
Crawford Drury ◽  
Carlo Caruso ◽  
Kate Quigley
Keyword(s):  
Coral Reefs ◽  
Thermal Tolerance ◽  
Selective Breeding ◽  
Marine Invertebrates ◽  
Association Studies ◽  
Current Evidence ◽  
Genome Wide Association Studies ◽  
Negative Effects ◽  
Important Species ◽  
Climate Action

The decline of coral reefs has prompted an emergent field of research on the potential for various biological interventions focused on increasing stress tolerance in corals. Among these is selective breeding, the selection and reproductive crossing of parental stock based on a trait of interest with the goal of enhancing the frequency or intensity of the trait in subsequent generations. Selective breeding has been successfully applied to commercially and ecologically important species to mitigate the negative effects of climate change, including marine invertebrates and more recently, corals. Here, we review the process of selective breeding and detail 4 case studies that have documented the increase of thermal tolerance in selectively bred corals across various life history stages and temperature stressors. These outcomes are supported by a substantial body of literature demonstrating the heritability of thermal tolerance across organisms, including genome wide association studies and family-specific responses to heat stress in larvae. We also highlight some of the major knowledge gaps around selective breeding, including the magnitude of possible phenotypic tradeoffs and the potential for unintended negative genetic consequences, and discuss how these risks can be mitigated. We conclude by suggesting conservation approaches that can benefit from the integration of selective breeding. Current evidence suggests that selective breeding may be a viable option for supporting the persistence of coral reefs while climate action develops.

scholarly journals Fetal Origins of Mental Disorders? An Answer Based on Mendelian Randomization

2018 ◽  
Vol 21 (6) ◽  
pp. 485-494 ◽  
Author(s):  
Subhi Arafat ◽  
Camelia C. Minică
Keyword(s):  
Mental Disorders ◽  
Observational Studies ◽  
Mendelian Randomization ◽  
Causal Effect ◽  
Association Studies ◽  
Current Evidence ◽  
Genome Wide Association Studies ◽  
Fetal Origins ◽  
Barker Hypothesis ◽  
Main Criticism

The Barker hypothesis states that low birth weight (BW) is associated with higher risk of adult onset diseases, including mental disorders like schizophrenia, major depressive disorder (MDD), and attention deficit hyperactivity disorder (ADHD). The main criticism of this hypothesis is that evidence for it comes from observational studies. Specifically, observational evidence does not suffice for inferring causality, because the associations might reflect the effects of confounders. Mendelian randomization (MR) — a novel method that tests causality on the basis of genetic data — creates the unprecedented opportunity to probe the causality in the association between BW and mental disorders in observation studies. We used MR and summary statistics from recent large genome-wide association studies to test whether the association between BW and MDD, schizophrenia and ADHD is causal. We employed the inverse variance weighted (IVW) method in conjunction with several other approaches that are robust to possible assumption violations. MR-Egger was used to rule out horizontal pleiotropy. IVW showed that the association between BW and MDD, schizophrenia and ADHD is not causal (all p > .05). The results of all the other MR methods were similar and highly consistent. MR-Egger provided no evidence for pleiotropic effects biasing the estimates of the effects of BW on MDD (intercept = -0.004, SE = 0.005, p = .372), schizophrenia (intercept = 0.003, SE = 0.01, p = .769), or ADHD (intercept = 0.009, SE = 0.01, p = .357). Based on the current evidence, we refute the Barker hypothesis concerning the fetal origins of adult mental disorders. The discrepancy between our results and the results from observational studies may be explained by the effects of confounders in the observational studies, or by the existence of a small causal effect not detected in our study due to weak instruments. Our power analyses suggested that the upper bound for a potential causal effect of BW on mental disorders would likely not exceed an odds ratio of 1.2.

scholarly journals Sparse Bayesian learning for predicting phenotypes and ranking influential markers in yeast

2018 ◽  
Author(s):  
Maryam Ayat ◽  
Michael Domaratzki
Keyword(s):  
Genomic Selection ◽  
Bayesian Learning ◽  
Association Studies ◽  
Kernel Functions ◽  
Genome Wide Association ◽  
Genome Wide Association Studies ◽  
Sparse Bayesian Learning ◽  
Negative Effects ◽  
String Kernels ◽  
Genome Wide

Genomic selection and genome-wide association studies are two related problems that can be applied to the plant breeding industry. Genomic selection is a method to predict phenotypes (i.e., traits) such as yield and drought resistance in crops from high-density markers positioned throughout the genome of the varieties. In this paper, we employ employ sparse Bayesian learning as a technique for genomic selection and ranking markers based on their relevance to a trait, which can aid in genome-wide association studies. We define and explore two different forms of the sparse Bayesian learning for predicting phenotypes and identifying the most influential markers of a trait, respectively. In particular, we introduce a new framework based on sparse Bayesian and ensemble learning for ranking influential markers of a trait. Then, we apply our methods on a real-world \textit{Saccharomyces cerevisiae} dataset, and analyse our results with respect to existing related works, trait heritability, as well as the accuracies obtained from the use of different kernel functions including linear, Gaussian, and string kernels. We find that sparse Bayesian methods are not only as good as other machine learning methods in predicting yeast growth in different environments, but are also capable of identifying the most important markers, including both positive and negative effects on the growth, from which biologists can get insight. This attribute can make our proposed ensemble of sparse Bayesian learners favourable in ranking markers based on their relevance to a trait.

scholarly journals Fear and Foxes: An Educational Primer for Use with “Anterior Pituitary Transcriptome Suggests Differences in ACTH Release in Tame and Aggressive Foxes”

Genetics ◽  
2020 ◽  
Vol 215 (1) ◽  
pp. 15-24 ◽  
Author(s):  
Julie H. Simpson
Keyword(s):  
Anterior Pituitary ◽  
Selective Breeding ◽  
Association Studies ◽  
Model Organisms ◽  
Genome Wide Association Studies ◽  
Behavioral Differences ◽  
Genetic Changes ◽  
Genome Wide ◽  
Discovery Science ◽  
Acth Release

The way genes contribute to behavior is complicated. Although there are some single genes with large contributions, most behavioral differences are due to small effects from many interacting genes. This makes it hard to identify the genes that cause behavioral differences. Mutagenesis screens in model organisms, selective breeding experiments in animals, comparisons between related populations with different behaviors, and genome-wide association studies in humans are promising and complementary approaches to understanding the heritable aspects of complex behaviors. To connect genes to behaviors requires measuring behavioral differences, locating correlated genetic changes, determining when, where, and how these candidate genes act, and designing causative confirmatory experiments. This area of research has implications from basic discovery science to human mental health.

Human individual radiation sensitivity and prospects for prediction

2018 ◽  
Vol 47 (3-4) ◽  
pp. 126-141 ◽  
Author(s):  
P. Rajaraman ◽  
M. Hauptmann ◽  
S. Bouffler ◽  
A. Wojcik
Keyword(s):  
Association Studies ◽  
High Sensitivity ◽  
Radiation Sensitivity ◽  
Ionising Radiation ◽  
Current Evidence ◽  
Genome Wide Association Studies ◽  
Low Doses ◽  
Stochastic Effects ◽  
Causal Pathway ◽  
Tissue Reactions

In the past few decades, it has become increasingly evident that sensitivity to ionising radiation is variable. This is true for tissue reactions (deterministic effects) after high doses of radiation, for stochastic effects following moderate and possibly low doses, and conceivably also for non-cancer effects such as cardiovascular disease, the causal pathway(s) of which are not yet fully understood. A high sensitivity to deterministic effects is not necessarily correlated with a high sensitivity to stochastic effects. The concept of individual sensitivity to high and low doses of radiation has long been supported by data from patients with certain rare hereditary conditions. However, these syndromes only affect a small proportion of the general population. More relevant to the majority of the population is the notion that some part of the genetic contribution defining radiation sensitivity may follow a polygenic model, which predicts elevated risk resulting from the inheritance of many low-penetrance risk-modulating alleles. Can the different forms of individual radiation sensitivities be inferred from the reaction of cells exposed ex vivo to ionising radiation? Can they be inferred from analyses of individual genotypes? This paper reviews current evidence from studies of late adverse tissue reactions after radiotherapy in potentially sensitive groups, including data from functional assays, candidate gene approaches, and genome-wide association studies. It focuses on studies published in 2013 or later because a comprehensive review of earlier studies was published previously in a report by the UK Advisory Group on Ionising Radiation.

Genetics of Depression

2017 ◽  
Author(s):  
Douglas F. Levinson ◽  
Walter E. Nichols
Keyword(s):  
Genetic Factors ◽  
Association Studies ◽  
Complex Trait ◽  
Current Evidence ◽  
Genome Wide Association Studies ◽  
Adverse Life Events ◽  
Major Depressive ◽  
Genome Wide ◽  
Increase Risk ◽  
And Function

Major depressive disorder (MDD) is a common and heterogeneous complex trait. Twin heritability is 35%–40%, perhaps higher in severe/recurrent cases. Adverse life events (particularly during childhood) increase risk. Current evidence suggests some overlap in genetic factors among MDD, bipolar disorder, and schizophrenia. Large genome-wide association studies (GWAS) are now proving successful. Polygenic effects of common SNPs are substantial. Findings implicate genes with effects on synaptic development and function, including two obesity-associated genes (NEGR1 and OLFM4), but not previous “candidate genes.” It can now be expected that larger GWAS samples will produce additional associations that shed new light on MDD genetics.

scholarly journals Mendelian randomization studies of biomarkers and type 2 diabetes

2015 ◽  
Vol 4 (4) ◽  
pp. 249-260 ◽  
Author(s):  
Ali Abbasi
Keyword(s):  
Type 2 Diabetes ◽  
Genetic Variants ◽  
Large Scale ◽  
Mendelian Randomization ◽  
Association Studies ◽  
Causal Effects ◽  
Current Evidence ◽  
Genome Wide Association Studies ◽  
Glycaemic Traits

Many biomarkers are associated with type 2 diabetes (T2D) risk in epidemiological observations. The aim of this study was to identify and summarize current evidence for causal effects of biomarkers on T2D. A systematic literature search in PubMed and EMBASE (until April 2015) was done to identify Mendelian randomization studies that examined potential causal effects of biomarkers on T2D. To replicate the findings of identified studies, data from two large-scale, genome-wide association studies (GWAS) were used: DIAbetes Genetics Replication And Meta-analysis (DIAGRAMv3) for T2D and the Meta-Analyses of Glucose and Insulin-related traits Consortium (MAGIC) for glycaemic traits. GWAS summary statistics were extracted for the same genetic variants (or proxy variants), which were used in the original Mendelian randomization studies. Of the 21 biomarkers (from 28 studies), ten have been reported to be causally associated with T2D in Mendelian randomization. Most biomarkers were investigated in a single cohort study or population. Of the ten biomarkers that were identified, nominally significant associations with T2D or glycaemic traits were reached for those genetic variants related to bilirubin, pro-B-type natriuretic peptide, delta-6 desaturase and dimethylglycine based on the summary data from DIAGRAMv3 or MAGIC. Several Mendelian randomization studies investigated the nature of associations of biomarkers with T2D. However, there were only a few biomarkers that may have causal effects on T2D. Further research is needed to broadly evaluate the causal effects of multiple biomarkers on T2D and glycaemic traits using data from large-scale cohorts or GWAS including many different genetic variants.

scholarly journals An integrated peach genome structural variation map uncovers genes associated with fruit traits

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Jian Guo ◽  
Ke Cao ◽  
Cecilia Deng ◽  
Yong Li ◽  
Gengrui Zhu ◽  
...  
Keyword(s):  
Agronomic Traits ◽  
Association Studies ◽  
Fruit Shape ◽  
Genomic Research ◽  
Genome Wide Association Studies ◽  
Structural Variations ◽  
Important Species ◽  
Peach Genome ◽  
Wide Range ◽  
Causal Variants

Abstract Background Genome structural variations (SVs) have been associated with key traits in a wide range of agronomically important species; however, SV profiles of peach and their functional impacts remain largely unexplored. Results Here, we present an integrated map of 202,273 SVs from 336 peach genomes. A substantial number of SVs have been selected during peach domestication and improvement, which together affect 2268 genes. Genome-wide association studies of 26 agronomic traits using these SVs identify a number of candidate causal variants. A 9-bp insertion in Prupe.4G186800, which encodes a NAC transcription factor, is shown to be associated with early fruit maturity, and a 487-bp deletion in the promoter of PpMYB10.1 is associated with flesh color around the stone. In addition, a 1.67 Mb inversion is highly associated with fruit shape, and a gene adjacent to the inversion breakpoint, PpOFP1, regulates flat shape formation. Conclusions The integrated peach SV map and the identified candidate genes and variants represent valuable resources for future genomic research and breeding in peach.

scholarly journals Epigenetics and the exposomes: Obesity and beyond

2013 ◽  
Vol 06 (03) ◽  
pp. 089-093
Author(s):  
Rita P. Raman ◽  
Anita D. Raman
Keyword(s):  
Environmental Factors ◽  
Association Studies ◽  
Adult Life ◽  
Genetic Alterations ◽  
Common Disease ◽  
Neural Function ◽  
Genome Wide Association Studies ◽  
Negative Effects ◽  
Environmental Signals ◽  
And Function

ABSTRACTThe specific genetic alterations that result in diseases and complex syndromes have been and continue to be identified. Search for the origins of disease have led to investigations into the roles of dietary and environmental factors as potential triggers or modifiers of risk. Genome-wide association studies have identified concepts such as the rare variant-common disease hypothesis and the common variant-common disease hypothesis.1 Through association studies, unique gene-environment interactions, which may occur with or without specific periods of permissiveness or vulnerabilities, have also been identified. Major conditions where the role of exposomes and epigenetics are rapidly evolving are obesity, neurological disorders, immune disorders and cancers. These concepts are particularly intriguing in the context of obesity. BACKGROUND: Epigenetics can be defined as heritable traits resulting from changes in DNA or chromatin structure without alterations in the DNA sequence.2 Nutritional epigenetics is seen as a means for the prevention of developmental diseases and cancer, and to delay processes associated with aging.3,4 Diseases in which epigenetic factors are considered significant include type 2 diabetes mellitus, obesity, inflammation, cardiovascular diseases, neurocognitive disorders, and immune diseases, with neural function influenced by environmental factors including early experience.5 Studies with rodent models suggest that during both early development and in adult life, environmental signals can activate intracellular pathways that directly remodel the epigenome, leading to changes in gene expression and function. These studies define a biological basis for the interplay between environmental signals and the genome in the regulation of individual differences in behavior, cognition, and physiology.6 In reproduction, certain genes are turned on while others are turned off in the process of imprinting. In the case of imprinting, even though there are two copies of the gene, only one copy is expressed and there is no substitute functional allele. For this reason, imprinting makes the imprinted genes more vulnerable to the negative effects of mutations.7

scholarly journals ABCA7 and Pathogenic Pathways of Alzheimer’s Disease

2018 ◽  
Vol 8 (2) ◽  
pp. 27 ◽  
Author(s):  
◽  
◽  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Association Studies ◽  
Amyloid Β ◽  
Current Evidence ◽  
Genome Wide Association Studies ◽  
In Vivo Models ◽  
Peripheral Tissues ◽  
Increased Risk ◽  
The Brain

The ATP-binding cassette (ABC) reporter family functions to regulate the homeostasis of phospholipids and cholesterol in the central nervous system, as well as peripheral tissues. ABCA7 belongs to the A subfamily of ABC transporters, which shares 54% sequence identity with ABCA1. While ABCA7 is expressed in a variety of tissues/organs, including the brain, recent genome-wide association studies (GWAS) have identified ABCA7 gene variants as susceptibility loci for late-onset Alzheimer’s disease (AD). More important, subsequent genome sequencing analyses have revealed that premature termination codon mutations in ABCA7 are associated with the increased risk for AD. Alzheimer’s disease is a progressive neurodegenerative disease and the most common cause of dementia, where the accumulation and deposition of amyloid-β (Aβ) peptides cleaved from amyloid precursor protein (APP) in the brain trigger the pathogenic cascade of the disease. In consistence with human genetic studies, increasing evidence has demonstrated that ABCA7 deficiency exacerbates Aβ pathology using in vitro and in vivo models. While ABCA7 has been shown to mediate phagocytic activity in macrophages, ABCA7 is also involved in the microglial Aβ clearance pathway. Furthermore, ABCA7 deficiency results in accelerated Aβ production, likely by facilitating endocytosis and/or processing of APP. Taken together, current evidence suggests that ABCA7 loss-of-function contributes to AD-related phenotypes through multiple pathways. A better understanding of the function of ABCA7 beyond lipid metabolism in both physiological and pathological conditions becomes increasingly important to explore AD pathogenesis.

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