Corrigendum: The zebrafish reference genome sequence and its relationship to the human genome

1] Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK [2].
Nature (Impact Factor: 41.46). 04/2013; 496(7446). DOI: 10.1038/nature12111
Source: PubMed


Zebrafish have become a popular organism for the study of vertebrate gene function. The virtually transparent embryos of this species, and the ability to accelerate genetic studies by gene knockdown or overexpression, have led to the widespread use of zebrafish in the detailed investigation of vertebrate gene function and increasingly, the study of human genetic disease. However, for effective modelling of human genetic disease it is important to understand the extent to which zebrafish genes and gene structures are related to orthologous human genes. To examine this, we generated a high-quality sequence assembly of the zebrafish genome, made up of an overlapping set of completely sequenced large-insert clones that were ordered and oriented using a high-resolution high-density meiotic map. Detailed automatic and manual annotation provides evidence of more than 26,000 protein-coding genes, the largest gene set of any vertebrate so far sequenced. Comparison to the human reference genome shows that approximately 70% of human genes have at least one obvious zebrafish orthologue. In addition, the high quality of this genome assembly provides a clearer understanding of key genomic features such as a unique repeat content, a scarcity of pseudogenes, an enrichment of zebrafish-specific genes on chromosome 4 and chromosomal regions that influence sex determination.

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Available from: Camille Berthelot, Sep 30, 2015
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    • "The study by Howe et al. also revealed a comparable number of species specific genes for zebrafish, human and mouse when duplicated genes are regarded as one gene (Howe et al., 2013). Teleost fish have undergone an additional round of whole genome duplication and although many of these duplicated ohnologs got subsequently lost, about 30% of all zebrafish genes still have one (Howe et al., 2013). The degree of conservation changes from gene to gene, and it remains to be determined in many cases whether both or only one of these duplicates are found in a given cell type. "
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    ABSTRACT: Myelin is the multi-layered membrane that surrounds most axons and is produced by oligodendrocytes in the central nervous system (CNS). In addition to its important role in enabling rapid nerve conduction, it has become clear in recent years that myelin plays additional vital roles in CNS function. Myelinating oligodendrocytes provide metabolic support to axons and active myelination is even involved in regulating forms of learning and memory formation. However, there are still large gaps in our understanding of how myelination by oligodendrocytes is regulated. The small tropical zebrafish has become an increasingly popular model organism to investigate many aspects of nervous system formation, function, and regeneration. This is mainly due to two approaches for which the zebrafish is an ideally suited vertebrate model-(1) in vivo live cell imaging using vital dyes and genetically encoded reporters, and (2) gene and target discovery using unbiased screens. This review summarizes how the use of zebrafish has helped understand mechanisms of oligodendrocyte behavior and myelination in vivo and discusses the potential use of zebrafish to shed light on important future questions relating to myelination in the context of CNS development, function and repair. GLIA 2015. © 2015 Wiley Periodicals, Inc.
    Glia 08/2015; DOI:10.1002/glia.22897 · 6.03 Impact Factor
    • "There are considerable strengths in using the zebrafish model to define mechanisms associated with developmental toxicant exposure and the developmental origins of adult health and disease including ex utero fertilization and embryonic development , rapid embryogenesis, and a relatively short life span. Paired with these biological strengths are the structural and functional homology of the zebrafish CNS to humans and the conserved genetic, molecular, and endocrine pathways making the zebrafish a powerful model to assess the later life alterations caused by an embryonic atrazine exposure (de Esch et al., 2012; Howe et al., 2013). There are a few recent studies that are now utilizing the zebrafish to examine the contributions of toxicant exposure to the DOHaD hypothesis. "
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    ABSTRACT: Atrazine is an herbicide applied to agricultural crops and is indicated to be an endocrine disruptor. Atrazine is frequently found to contaminate potable water supplies above the maximum contaminant level of 3μg/L as defined by the U. S. Environmental Protection Agency. The developmental origin of adult disease hypothesis suggests that toxicant exposure during development can increase the risk of certain diseases during adulthood. However, the molecular mechanisms underlying disease progression are still unknown. In this study, zebrafish embryos were exposed to 0, 0.3, 3, or 30μg/L atrazine throughout embryogenesis. Larvae were then allowed to mature under normal laboratory conditions with no further chemical treatment until 7 days post fertilization (dpf) or adulthood and neurotransmitter analysis completed. No significant alterations in neurotransmitter levels was observed at 7 dpf or in adult males, but a significant decrease in 5-Hydroxyindoleacetic acid (5-HIAA) and serotonin turnover was seen in adult female brain tissue. Transcriptomic analysis was completed on adult female brain tissue to identify molecular pathways underlying the observed neurological alterations. Altered expression of 1853, 84, and 419 genes in the females exposed to 0.3, 3, or 30μg/L atrazine during embryogenesis were identified, respectively. There was a high level of overlap between the biological processes and molecular pathways in which the altered genes were associated. Moreover, a subset of genes was down regulated throughout the serotonergic pathway. These results provide support of the developmental origins of neurological alterations observed in adult female zebrafish exposed to atrazine during embryogenesis. Copyright © 2015. Published by Elsevier Ireland Ltd.
    Toxicology 04/2015; 333. DOI:10.1016/j.tox.2015.04.016 · 3.62 Impact Factor
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    • "4.1. Using zebrafish to model human neurobehavioral disorders 82% of human related disease genes are present in the zebrafish genome (Howe et al., 2013). And zebrafish physiology is very similar to ours (Bakkers, 2011; Gestri et al., 2012). "
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    ABSTRACT: Obsessive-Compulsive Disorder (OCD) is the tenth most disabling illness of any kind. OCD stands as a paradigm for complex neurobehavioral disorders due to its polygenic origin. It presents heterogenic clinical presentation, variable disease onset, progression and treatment responses, what makes its understanding a major neuropsychiatric challenge. Like with other neurobehavioral disorders, animal models are essential tools for decoding OCD genetic complexity, understanding its biological base and discovering novel treatments and diagnostic methods. 20 years of rodent OCD modeling have helped to understand the disease better, but multiple questions remain regarding OCD. Innovative whole genome sequencing (WGS) approaches might provide important answers on OCD risk associated genes. However, exploiting those large data sets through the use of traditional animal models is costly and time consuming. Zebrafish might be an appropriate animal model to streamline the pipeline of gene functional validation. This animal model shows several advantages versus rodent models, such as faster and cheaper genetic manipulation, strong impact on the 3Rs implementation, behavioral phenotypic reproducibility of OCD-like behaviors (obsessions and compulsions) and feasibility to develop high-throughput assays for novel OCD drug therapies discovery. In conclusion, zebrafish could be an innovative and relevant model for understanding OCD. Copyright © 2015 Elsevier B.V. All rights reserved.
    European journal of pharmacology 03/2015; 759. DOI:10.1016/j.ejphar.2015.03.027 · 2.53 Impact Factor
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