Epimutations in developmental genes underlie the onset of domestication in farmed European sea bass
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ABSTRACT:
PROVIDER: PRJNA515290 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8444950.fastq.gz | Fastqsanger.gz | |||
| SRR8444960.fastq.gz | Fastqsanger.gz | |||
| SRR8444970_1.fastq.gz | Fastqsanger.gz | |||
| SRR8444970_2.fastq.gz | Fastqsanger.gz | |||
| SRR8444980_1.fastq.gz | Fastqsanger.gz |
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Project description:Domestication of wild animals induces a set of phenotypic characteristics collectively known as the domestication syndrome. However, how this syndrome emerges is still not clear. Recently, the neural crest cell deficit hypothesis proposed that it is generated by a mildly disrupted neural crest cell developmental program, but clear support is lacking due to the difficulties of distinguishing pure domestication effects from preexisting genetic differences between farmed and wild mammals and birds. Here, we use a farmed fish as model to investigate the role of persistent changes in DNA methylation (epimutations) in the process of domestication.We show that early domesticates of sea bass, with no genetic differences with wild counterparts, contain epimutations in tissues with different embryonic origins. About one fifth of epimutations that persist into adulthood are established by the time of gastrulation and affect genes involved in developmental processes that are expressed in embryonic structures, including the neural crest. Some of these genes are differentially expressed in sea bass with lower jaw malformations, a key feature of domestication syndrome. Interestingly, these epimutations significantly overlap with cytosine-to-thymine polymorphisms after 25 years of selective breeding. Furthermore, epimutated genes coincide with genes under positive selection in other domesticates. We argue that the initial stages of domestication include dynamic alterations in DNA methylation of developmental genes that affect the neural crest. Our results suggest a role for epimutations during the beginning of domestication that could be fixed as genetic variants and suggest a conserved molecular process to explain Darwin’s domestication syndrome across vertebrates.
2019-07-09 | GSE125124 | GEO
Project description:Domestication of wild animals induces a set of phenotypic characteristics collectively known as the domestication syndrome. However, how this syndrome emerges is still not clear. Recently, the neural crest cell deficit hypothesis proposed that it is generated by a mildly disrupted neural crest cell developmental program, but clear support is lacking due to the difficulties of distinguishing pure domestication effects from preexisting genetic differences between farmed and wild mammals and birds. Here, we use a farmed fish as model to investigate the role of persistent changes in DNA methylation (epimutations) in the process of domestication. We show that early domesticates of sea bass, with no genetic differences with wild counterparts, contain epimutations in tissues with different embryonic origins. About one fifth of epimutations that persist into adulthood are established by the time of gastrulation and affect genes involved in developmental processes that are expressed in embryonic structures, including the neural crest. Some of these genes are differentially expressed in sea bass with lower jaw malformations, a key feature of domestication syndrome. Interestingly, these epimutations significantly overlap with cytosine-to-thymine polymorphisms after 25 years of selective breeding. Furthermore, epimutated genes coincide with genes under positive selection in other domesticates. We argue that the initial stages of domestication include dynamic alterations in DNA methylation of developmental genes that affect the neural crest. Our results indicate a role for epimutations during the beginning of domestication that could be fixed as genetic variants and suggest a conserved molecular process to explain Darwin's domestication syndrome across vertebrates.
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Project description:Due to multi-generation domestication selection, farmed and wild Atlantic salmon diverge genetically, which raises concerns about potential genetic interactions among escaped farmed and wild populations and disrupts local adaptation through introgression. When farmed strains of distant geographic origin are used, it is unknown whether the genetic risks posed by escaped farmed fish will be greater than if more locally derived strains are used. Quantifying gene expression differences among divergent farmed, wild and F1 hybrids under controlled conditions is one of the ways to explore the consequences of hybridization. We compared the transcriptomes of late sac fry of a European (EO) farmed (“StofnFiskur”, Norwegian strain), a North American (NA) farmed (Saint John River, NB strain), a Newfoundland (NF) wild population with EO ancestry, and related F1 hybrids using 44K microarrays. Our findings indicate that the wild population showed greater transcriptome differences from the EO farmed strain than that of the NA farmed strain. We also found the largest differences in global gene expression between the two farmed strains. We detected fewer differentially expressed transcripts between F1 hybrids and domesticated/wild maternal strains. We also found that the differentially expressed genes between cross types over-represented GO terms associated with metabolism, development, growth, immune response, and redox homeostasis processes. These findings suggest that the interbreeding of escaped EO/NA farmed and NF wild population would alter gene transcription, and the consequences of hybridization would be greater from escaped EO farmed than NA farmed salmon, resulting in potential effects on the fitness of wild populations.
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Project description:The application of genome sequencing in patients with intellectual disability and congenital anomalies (ID/CA) typically identifies causative mutations only in a minority of cases. We hypothesized that some cases of ID/CA are caused by epigenetic aberrations that dysregulate normal genome function, and that these would be missed by conventional sequencing approaches. We performed Illumina 450k DNA methylation profiling in ~500 individuals with ID/CA, who were negative for causative mutations by microarray, exome- and/or whole genome sequencing. We screened patient methylation profiles for epimutations absent in ~1,500 controls, and validated these by bisulfite sequencing, revealing that epimutations represent large methylation changes specifically on one allele. Parental studies show that approximately half represent de novo events, a rate significantly higher than that seen in controls. We identified seven recurrent events, two of which (FMR1, MEG3) have known disease associations, validating our method for detecting pathogenic epimutations. From large-scale sequencing, population and expression studies we conclude that epimutations are: (i) Frequently associated with extreme outlier and mono-allelic gene expression, with an impact comparable to loss-of-function mutations; (ii) Generally conserved across multiple tissues within an individual, validating the use of blood DNA to study ID/CA; (iii) Can occur secondary to cis-linked regulatory mutations, providing a rationale for interpreting non-coding genetic variants; (iv) Occur sporadically with a remarkably high de novo rate, and (v) Exhibit non-Mendelian inheritance, likely being reset between generations by epigenetic reprogramming during embryogenesis. We conclude that epimutations underlie 5-10% of patients with ID/CA who are refractory to conventional mutation screening, and propose that epigenome profiling represents a promising method for the study of human disease that complements sequence-based approaches.
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Project description:H3K27me3 demethylases and epimutations
| PRJEB36508 | ENA
Project description:Epigenetic inheritance is the transmission of altered gene expression states across dividing cells without DNA sequence variation. Induced epigenetic changes (epimutations) have been extensively studied, but importantly, epimutations also occur spontaneously in a manner reminiscent of DNA sequence change. Small RNAs are established as a source of spontaneous epimutations which transmit gene expression changes over multiple generations in C.elegans. These changes are generally short lived, but rarely long-lived changes occur. Given that chromatin state is a critical regulator of gene expression, we explored whether chromatin states also undergo spontaneous change and whether this could be a potential alternative mechanism for transgenerational epigenetic inheritance. We compared the chromatin profiles and gene expression profiles at matched time points from a twenty generation bottlenecked lineage of C.elegans. We found that heritable changes in gene expression arose at a higher rate than the estimate for DNA sequence variation, indicating that these were true epigenetic events. In addition to recapitulating the known role for small RNAs, we provide evidence for chromatin mediated epimutations as an alternative mechanism driving epigenetic inheritance. Chromatin epimutations were heritable, enriched in the germline and synchronised with inherited gene expression changes. As with small RNA mediated epimutations, they were generally short lived with a tendency to resolve to baseline after 2-3 generations. A subset of chromatin epimutations however were long lasting, and these were uniquely enriched in piRNA clusters. Genes with long lived epimutations were implicated in multiple components of xenobiotic response pathways. This points to a mechanism for epigenetic ‘anticipation’ of environmental stressors. Adaptive traits driven by epimutations may be selected for under adverse conditions and lost on return to normal conditions, enabling soft adaptation in the absence of genetic sequence change.
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