genesis Journal Impact Factor & Information

Publisher: Wiley

Journal description

We have crossed the threshold into a new age of research in developmental biology. As the international genome project enters its climatic phase, new research generates an unprecedented amount of information on the sequence and identification of genes and their structure. We soon anticipate the existence of a 'book of life': a comprehensive catalogue of all known genes together with their nucleotide sequence. This new dawn calls for a pioneering new journal offering new approaches and perspectives for understanding the function of genes and the roles they play in complex biological processes, both individually and in combination at the molecular, cellular, organismal and population level. On January 1, 2000, we became the editors of the journal Developmental Genetics, published by Wiley (New York). The focus of the journal is on the genetics of development and fundamental embryological research resulting from studies in animals and plants. We publish pioneering articles offering new perspectives on all model genetic systems to understand the function of genes, alone and in combination, acknowledging the multigenic character of complex biological processes. Contributions using non-traditional animal and plant systems are encouraged to emphasize the journal's interest in comparative studies. Special attention is also given to technology-oriented reports. We invite you to contribute to genesis. We welcome submissions in the form of letters, articles, correspondence, and technology updates, which advance knowledge across a range of dynamic areas on the cutting edge of developmental biology, including mutagenesis; embryogenesis; histeogenesis; morphogenesis; organogenesis.

Current impact factor: 2.02

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 2.018
2013 Impact Factor 2.042
2012 Impact Factor 2.584
2011 Impact Factor 2.527
2010 Impact Factor 2.395
2009 Impact Factor 2.223
2008 Impact Factor 2.217

Impact factor over time

Impact factor

Additional details

5-year impact 2.41
Cited half-life 8.80
Immediacy index 0.45
Eigenfactor 0.01
Article influence 1.18
Website Genesis website
Other titles Genesis (New York, N.Y.: 2000: Online), Genesis
ISSN 1526-968X
OCLC 42463257
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo
  • Conditions
    • Some journals have separate policies, please check with each journal directly
    • On author's personal website, institutional repositories, arXiv, AgEcon, PhilPapers, PubMed Central, RePEc or Social Science Research Network
    • Author's pre-print may not be updated with Publisher's Version/PDF
    • Author's pre-print must acknowledge acceptance for publication
    • Non-Commercial
    • Publisher's version/PDF cannot be used
    • Publisher source must be acknowledged with citation
    • Must link to publisher version with set statement (see policy)
    • If OnlineOpen is available, BBSRC, EPSRC, MRC, NERC and STFC authors, may self-archive after 12 months
    • If OnlineOpen is available, AHRC and ESRC authors, may self-archive after 24 months
    • Publisher last contacted on 07/08/2014
    • This policy is an exception to the default policies of 'Wiley'
  • Classification
    ​ yellow

Publications in this journal

  • Jeremy T Baeten · Ashley R Jackson · Kirk M McHugh · Brenda Lilly
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    ABSTRACT: The overlapping roles of the predominant Notch receptors in vascular smooth muscle cells, Notch2 and Notch3, have not been clearly defined in vivo. In this study, we use a smooth muscle-specific deletion of Notch2 together with a global Notch3 deletion to produce mice with combinations of mutant and wild-type Notch2/3 alleles in vascular smooth muscle cells. Mice with complete loss of Notch3 and smooth muscle-expressed Notch2 display late embryonic lethality and subcutaneous hemorrhage. Mice without smooth muscle-Notch2 and only one wild-type copy of Notch3 die within one day of birth and present with vascular defects, most notably patent ductus arteriosus and aortic dilation. These defects were associated with decreased expression of contractile markers in both the ductus arteriosus and aorta. These results demonstrate that Notch2 and Notch3 have overlapping roles in promoting development of vascular smooth muscle cells, and together contribute to functional closure of the ductus arteriosus. This article is protected by copyright. All rights reserved.
    genesis 10/2015; DOI:10.1002/dvg.22904
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    ABSTRACT: We have established a novel Cre mouse line, using genomic elements encompassing the Nrp2 locus, present within a bacterial artificial chromosome (BAC) clone. By crossing this Cre driver line to R26R LacZ reporter mice, we have documented the temporal expression and lineage traced tissues in which Cre is expressed. Nrp2-Cre drives expression in primitive blood cells arising from the yolk sac, venous and lymphatic endothelial cells, peripheral sensory ganglia and the lung bud. This mouse line will provide a new tool to researchers wishing to study the development of various tissues and organs in which this Cre driver is expressed, as well as allow tissue-specific knockout of genes of interest to study protein function. This work also presents the first evidence for expression of Nrp2 protein in a mesodermal progenitor with restricted hematopoietic potential, which will significantly advance the study of primitive erythropoiesis. This article is protected by copyright. All rights reserved.
    genesis 10/2015; DOI:10.1002/dvg.22905
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    ABSTRACT: Biological significance of the globin protein family could be ascertained by their conservation through archaea to human. Globin(s) have been "classically" studied as oxygen binding protein(s), with recent implications in a host of other physiological functions. Drosophila melanogaster possesses three globin genes (glob1, glob2, glob3) located at different cytogenetic positions. We have performed a comprehensive investigation on the cellular expression profile and functional relevance of glob1 in Drosophila development. A profound level of maternally contributed glob1 gene products was found during early embryogenesis. Subsequently, commencement of zygotic transcription leads to its strong expression in somatic muscles, gut primordia, fat bodies, tracheal cells, etc. Similarly, dynamic expression of glob1 was evident in most of the larval tissues, interestingly with high expression in dividing cells. Reduced expression of glob1 leads to various impairments and lethality during embryogenesis and larval development. Subsequently, a substantial increase in level of cellular ROS was also evident due to reduced expression of glob1 which consequently leads to locomotor impairment and early aging in surviving adult flies. To best of our knowledge, this is the first report which demonstrates that in addition to oxygen management, globin gene(s) are also involved in regulating various aspects of development in Drosophila. This article is protected by copyright. All rights reserved.
    genesis 10/2015; DOI:10.1002/dvg.22902
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    ABSTRACT: The Otx2 homeodomain transcription factor exerts multiple functions in specific developmental contexts, likely through the regulation of different sets of genes. Protein partners of Otx2 have been shown to modulate its activity. Therefore, the Otx2 interactome may play a key role in selecting a precise target-gene repertoire, hence determining its function in a specific tissue. To address the nature of Otx2 interactome, we generated of a new recombinant Otx2(CTAP-tag) mouse line, designed for protein complexes purification. We validated this mouse line by establishing the Otx2 interactome in the adult neural retina. In this tissue, Otx2 is thought to have overlapping function with its paralog Crx. Our analysis revealed that, contrary to Crx, Otx2 did not develop interactions with proteins known to regulate phototransduction genes but showed specific partnership with factors associated with retinal development. The relationship between Otx2 and Crx in the neural retina should therefore be considered as complementarity rather than redundancy. Furthermore, study of the Otx2 interactome revealed strong associations with RNA processing and translation machineries, suggesting unexpected roles for Otx2 in the regulation of selected target genes all along the transcription/translation pathway. The Otx2(CTAP-tag) line therefore appears suitable for a systematic approach to Otx2 protein-protein interactions. This article is protected by copyright. All rights reserved.
    genesis 10/2015; DOI:10.1002/dvg.22903
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    ABSTRACT: Maintenance of genome integrity is crucial for the germline, and this is reflected by lower mutation rates in gametes than somatic cells. Germ cells at different stages employ different DNA damage response (DDR) mechanisms. In response to certain DNA repair defects, primordial germ cells (PGCs) either undergo apoptosis or delayed proliferation, although little is known about the underlying mechanisms that govern these outcomes. Here, we report genetic studies of DDR pathways that underlie germ cell depletion in mice mutant for minichromosome maintenance 9 (Mcm9), a gene that plays a role in homologous recombination repair (HRR). Germ cell depletion in these mice is a result of reduced PGC numbers both before and after they arrive in the primitive gonads. This reduction was attributable to reduced proliferation, not apoptosis, and this response was independent of ATM-CHK2-TRP53-P21 signaling. This mechanism of PGC depletion differs from that in Fancm mutants, which also display reduced PGC depletion that is partially orchestrated by the ATM-TRP53-P21 pathway. Germ cell depletion in mice doubly deficient for FANCM and MCM9 was additive, indicating that the damage caused by each mutation triggers different DDR pathways to slow the cell cycle as a means to preserve genomic integrity. This article is protected by copyright. All rights reserved.
    genesis 09/2015; DOI:10.1002/dvg.22901
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    ABSTRACT: The cre/loxP recombination system is a valuable tool used to generate tissue specific genomic rearrangements in mouse models. The deletion of a region of interest flanked by two loxP sites is accomplished by the recombinase (cre) enzyme, which binds to the inverted repeat segments of two loxP sites and recognition of a conserved TA sequence in the asymmetric central spacer region "ATAACTTCGTATA -NNNTANNN-TATACGAAGTTAT. In vivo, we found that a single T to C mutation at position 4 of the central spacer region in the distal (3') loxP site, completely inhibited the recombination reaction in two conditional mouse models. These mice were generated using a mitochondrial methionyl-tRNA formyltransferase (Mtfmt) gene targeted construct and cre transgene under the control of tissue-specific promoters: calcium/calmodulin-dependent kinase II alpha (Camk2a-cre) and myosin light polypeptide 1 (Myl1-cre). Surprisingly, transient transfection of a plasmid expressing cre in dermal fibroblasts derived from the same mutant floxed Mtfmt((loxP/loxP)) mice line, successfully deleted the region of interest. This study demonstrates the sequence specificity required in vivo, the possibility of bypassing this limitation by expressing high levels of cre recombinase ex vivo and raises concerns related to the quality control of large scale production of gene targeted constructs and mice. This article is protected by copyright. All rights reserved. © 2015 Wiley Periodicals, Inc.
    genesis 09/2015; DOI:10.1002/dvg.22899
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    ABSTRACT: The domesticated zebra finch (Taeniopygia guttata) is a well-established animal model for studying vocal learning. It is also a tractable model for developmental analyses. The finch genome has been sequenced and methods for its transgenesis have been reported. Hatching and sexual maturation in this species takes only two weeks and three months, respectively. Finch colonies can be established relatively easily and its eggs are laid at a stage earlier than in other common avian experimental models, facilitating the analysis of very early avian development. Representing the Neoaves to which 95% of all bird species belong, the finch can potentially complement two existing, Galloanserae developmental models, the chick and quail. Here, we provide a step-by-step guide for how to set up a finch colony in a conventional lab environment. Technical tips are offered to optimize hens' productivity and ensure a constant supply of fertilized finch eggs. Methods of handling finch eggs and embryos for subsequent embryological, cellular or molecular analyses are also discussed. We conclude by emphasizing scientific values and cost effectiveness of maintaining a finch colony for avian developmental studies. This article is protected by copyright. All rights reserved.
    genesis 09/2015; DOI:10.1002/dvg.22900
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    ABSTRACT: The CAP superfamily member, CRISPLD2, has previously been shown to be associated with nonsyndromic cleft lip and palate (NSCL/P) in human populations and to be essential for normal craniofacial development in the zebrafish. Additionally, in rodent models, CRISPLD2 has been shown to play a role in normal lung and kidney development. However, the specific role of CRISPLD2 during these developmental processes has yet to be determined. In this study, we demonstrate that Crispld2 protein localizes to the orofacial region of the zebrafish embryo and knockdown of crispld2 results in abnormal migration of neural crest cells during both early and late time points. We also show an increase in cell death after crispld2 knockdown as well as an increase in apoptotic marker genes. Our data suggests that Crispld2 modulates the migration, differentiation and/or survival of NCCs during early craniofacial development. These results indicate an important role for Crispld2 in neural crest cell migration during craniofacial development and suggests involvement of Crispld2 in cell viability during formation of the orofacies. This article is protected by copyright. All rights reserved. © 2015 Wiley Periodicals, Inc.
    genesis 08/2015; DOI:10.1002/dvg.22897
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    ABSTRACT: Although sea urchin gastrulation is well described at the cellular level, our understanding of the molecular changes that trigger the coordinated cell movements involved is not complete. Jun N-terminal kinase (JNK) is a component of the planar cell polarity pathway and is required for cell movements during embryonic development in several animal species. To study the role of JNK in sea urchin gastrulation, embryos were treated with JNK inhibitor SP600125 just prior to gastrulation. The inhibitor had a limited and specific effect, blocking invagination of the archenteron. Embryos treated with 2uM SP600125 formed normal vegetal plates, but did not undergo invagination to form an archenteron. Other types of cell movements, specifically ingression of the skeletogenic mesenchyme, were not affected, although the development and pattern of the skeleton was abnormal in treated embryos. Pigment cells, derived from non-skeletogenic mesenchyme, were also present in SP600125 treated embryos. Despite the lack of a visible archenteron in treated embryos, cells at the original vegetal plate expressed several molecular markers for endoderm differentiation. These results demonstrate that JNK activity is required for invagination of the archenteron but not its differentiation, indicating that in this case, morphogenesis and differentiation are under separate regulation. This article is protected by copyright. All rights reserved. © 2015 Wiley Periodicals, Inc.
    genesis 08/2015; DOI:10.1002/dvg.22898
  • genesis 08/2015; 53(8):449. DOI:10.1002/dvg.22882
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    ABSTRACT: Single Nucleotide Polymorphisms in FTO intron 1 have been associated with obesity risk, leading to the hypothesis that FTO is the obesity-related gene. However, other studies have shown that the FTO gene is part of the regulatory domain of the neighboring IRX3 gene and that enhancers in FTO intron 1 regulate IRX3. While Irx3 activity was shown to be necessary in the hypothalamus for the metabolic function of Irx3 in mouse, no enhancers with hypothalamic activity have been demonstrated in the risk-associated region within FTO. In order to identify potential enhancers at the human FTO locus in vivo, we tested regulatory activity in FTO intron 1 using BAC transgenesis in zebrafish. A minimal gata2 promoter-GFP cassette was inserted 1.3 kb upstream of the obesity associated SNP rs9939609 in a human FTO BAC plasmid. In addition to the previously identified expression domains in notochord and kidney, human FTO BAC:GFP transgenic zebrafish larvae expressed GFP in the ventral posterior tuberculum, the posterior hypothalamus and the anterior brainstem, which are also expression domains of zebrafish irx3a. In contrast, an in-frame insertion of a GFP cassette at the FTO start codon resulted in weak ubiquitous GFP expression indicating that the promoter of FTO does likely not react to enhancers located in the obesity risk-associated region. This article is protected by copyright. All rights reserved. © 2015 Wiley Periodicals, Inc.
    genesis 08/2015; DOI:10.1002/dvg.22884
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    ABSTRACT: A complex network of transcription factors regulates specification of neural crest cells at early neurula stage by stabilizing neural crest identity and activating neural crest effector genes so that distinct subpopulations evolve. In this network c-myc acts on top of the gene hierarchy controlling snail2, AP2 and prohibitin1 (phb1) expression. While snail2 and AP2 are well studied neural crest specifier genes little is known about the role of phb1 in this process. To identify phb1 regulated genes we analyzed the transcriptome of neural crest explants of phb1 morphant Xenopus embryos. Among 147 phb1 regulated genes we identified the membrane associated protein-tyrosine phosphatase PRP4A3 (prl3) and the atypical cadherin and Wnt-PCP component van gogh like1 (vangl1). Gain of function, loss of function and epistasis experiments allowed us to allocate both genes in the neural crest specification network between phb1 and twist. Interestingly, both, vangl1 and prl3 regulate only a small subset of neural crest marker genes. The identification of two membrane associated proteins as novel neural crest specifiers indicates that in addition to gene regulation by combinatory effects of transcription factors also post-translational modifications (prl3) and cell-cell adhesion and/or regulation of cell-polarity (vangl1) specify the identity of neural crest cell populations. This article is protected by copyright. All rights reserved. © 2015 Wiley Periodicals, Inc.
    genesis 08/2015; DOI:10.1002/dvg.22883
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    ABSTRACT: The neural-epidermal boundary tissues include the neural crest and preplacodal ectoderm (PPE) as primordial constituents. The PPE region is essential for the development of various sensory and endocrine organs, such as the anterior lobe of the pituitary, olfactory epithelium, lens, trigeminal ganglion, and otic vesicles. During gastrulation, a neural region is induced in ectodermal cells that interacts with mesendodermal tissue and responds to several secreted factors. Among them, inhibition of bone morphogenetic protein (BMP) in the presumptive neuroectoderm is essential for the induction of neural regions, and formation of a Wnt and fibroblast growth factor (FGF) signaling gradient along the midline determines anterior-posterior patterning. In this study, we attempted to specifically induce PPE cells from undifferentiated Xenopus cells by regulating BMP, Wnt and FGF signaling. We showed that the proper level of BMP inhibition with an injection of truncated BMP receptor or treatment with a chemical antagonist triggered the expression of PPE genes. In addition, by varying the amount of injected chordin, we optimized specific expression of the PPE genes. PPE gene expression increased by adding an appropriate dose of a FGF receptor antagonist. Furthermore, co-injection with either wnt8 or the Wnt inhibitor dkk-1 altered the expression levels of several region-specific genes according to the injected dose. We specifically induced PPE cell differentiation in animal cap cells from early-stage Xenopus embryos by modulating BMP, Wnt and FGF signaling. This is not the first research on placode induction, but our simple method could potentially be applied to mammalian stem cell systems. This article is protected by copyright. All rights reserved. © 2015 Wiley Periodicals, Inc.
    genesis 08/2015; DOI:10.1002/dvg.22881
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    ABSTRACT: RFX transcription factors are key regulators of ciliogenesis in vertebrates. In Xenopus and zebrafish embryos, knockdown of Rfx2 causes defects in neural tube closure and in left-right axis patterning. To determine the essential role of the Rfx2 gene in mammalian development, we generated Rfx2-deficient mice using an embryonic stem cell clone containing a lacZ gene trap reporter inserted into the first intron of the Rfx2 gene. We found that the Rfx2 lacZ reporter is expressed in ciliated tissues during mouse development including the node, the floor plate and the dorsal neural tube. However, mice homozygous for the Rfx2 gene trap mutation did not have defects in neural tube closure or in organ situs. The gene trap insertion appears to create a null allele as Rfx2 mRNA was not detected in Rfx2(gt/gt) embryos. Although Rfx2-deficient mice do not have an obvious embryonic phenotype, we found that Rfx2(gt/gt) males are infertile due to a defect in spermatid maturation at or before the round and elongating spermatid stage. Our results indicate that Rfx2 is not essential for embryonic development in the mouse but is required for spermatogenesis. This article is protected by copyright. All rights reserved. © 2015 Wiley Periodicals, Inc.
    genesis 08/2015; DOI:10.1002/dvg.22880
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    ABSTRACT: The abundance of phenotypic diversity among species can enrich our knowledge of development and genetics beyond the limits of variation that can be observed in model organisms. The Phenoscape Knowledgebase (KB) is designed to enable exploration and discovery of phenotypic variation among species. Because phenotypes in the KB are annotated using standard ontologies, evolutionary phenotypes can be compared with phenotypes from genetic perturbations in model organisms. To illustrate the power of this approach, we review the use of the KB to find taxa showing evolutionary variation similar to that of a query gene. Matches are made between the full set of phenotypes described for a gene and an evolutionary profile, the latter of which is defined as the set of phenotypes that are variable among the daughters of any node on the taxonomic tree. Phenoscape's semantic similarity interface allows the user to assess the statistical significance of each match and flags matches that may only result from differences in annotation coverage between genetic and evolutionary studies. Tools such as this will help meet the challenge of relating the growing volume of genetic knowledge in model organisms to the diversity of phenotypes in nature. The Phenoscape KB is available at This article is protected by copyright. All rights reserved. © 2015 Wiley Periodicals, Inc.
    genesis 07/2015; 53(8). DOI:10.1002/dvg.22878
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    ABSTRACT: Ellis-van Creveld (EvC) syndrome (OMIM 225500) is an autosomal recessive disease characterized with chondrodysplastic dwarfism in association with abnormalities in oral cavity. Ciliary proteins EVC and EVC2 have been identified as causative genes and they play an important role on Hedgehog signal transduction. We have also identified a causative gene LIMBIN for bovine chondrodysplastic dwarfism (bcd) that is later identified as the bovine ortholog of EVC2. Here, we report generation of conventional and conditional mutant Evc2/Limbin alleles that mimics mutations found in EvC patients and bcd cattle. Resulted homozygous mice showed no ciliary localization of EVC2 and EVC and displayed reduced Hedgehog signaling activity in association with skeletal and oral defects similar to the EvC patients. Cartilage-specific disruption of Evc2/Limbin resulted in similar but milder skeletal defects, whereas osteoblast-specific disruption did not cause overt changes in skeletal system. Neural crest-specific disruption of Evc2/Limbin resulted in defective incisor growth similar to that seen in conventional knockouts; however, differentiation of amelobolasts was relatively normal in the conditional knockouts. These results showcased functions of EVC2/LIMBIN during formation of mineralized tissues. Availability of the conditional allele for this gene should facilitate further detailed analyses of the role of EVC2/LIMBIN in pathogenesis of EvC syndrome. This article is protected by copyright. All rights reserved. © 2015 Wiley Periodicals, Inc.
    genesis 07/2015; DOI:10.1002/dvg.22879
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    ABSTRACT: The Arabidopsis Information Resource (TAIR) is a continuously updated, online database of genetic and molecular biology data for the model plant Arabidopsis thaliana that provides a global research community with centralized access to data for over 30,000 Arabidopsis genes. TAIR's biocurators systematically extract, organize, and interconnect experimental data from the literature along with computational predictions, community submissions, and high throughput datasets to present a high quality and comprehensive picture of Arabidopsis gene function. TAIR provides tools for data visualization and analysis, and enables ordering of seed and DNA stocks, protein chips and other experimental resources. TAIR actively engages with its users who contribute expertise and data that augments the work of the curatorial staff. TAIR's focus in an extensive and evolving ecosystem of online resources for plant biology is on the critically important role of extracting experimentally-based research findings from the literature and making that information computationally accessible. In response to the loss of government grant funding, the TAIR team founded a nonprofit entity, Phoenix Bioinformatics, with the aim of developing sustainable funding models for biological databases, using TAIR as a test case. Phoenix has successfully transitioned TAIR to subscription-based funding while still keeping its data relatively open and accessible. This article is protected by copyright. All rights reserved. © 2015 Wiley Periodicals, Inc.
    genesis 07/2015; 53(8). DOI:10.1002/dvg.22877
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    ABSTRACT: Grainyhead-like genes are part of a highly conserved gene family that play a number of roles in ectoderm development and maintenance in mammals. Here we identify a novel allele of Grhl2, cleft-face 3 (clft3), in a mouse line recovered from an ENU mutagenesis screen for organogenesis defects. Homozygous clft3 mutants have a number of phenotypes in common with other alleles of Grhl2. We note a significant effect of genetic background on the clft3 phenotype. One of these is a reduction in size of the telencephalon where we find abnormal patterns of neural progenitor mitosis and apoptosis in mutant brains. Interestingly, Grhl2 is not expressed in the developing forebrain, suggesting this is a survival factor for neural progenitors exerting a paracrine effect on the neural tissue from the overlying ectoderm where Grhl2 is highly expressed. This article is protected by copyright. All rights reserved. © 2015 Wiley Periodicals, Inc.
    genesis 07/2015; DOI:10.1002/dvg.22875
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    ABSTRACT: Xenbase, the Xenopus model organism database (, is a cloud-based, web accessible resource that integrates the diverse genomic and biological data from Xenopus research. Xenopus frogs are one of the major vertebrate animal models used for biomedical research, and Xenbase is the central repository for the enormous amount of data generated using this model tetrapod. The goal of Xenbase is to accelerate discovery by enabling investigators to make novel connections between molecular pathways in Xenopus and human disease. Our relational database and user-friendly interface make these data easy to query, and allows investigators to quickly interrogate and link different data types in ways that would otherwise be difficult, time consuming, or impossible. Xenbase also enhances the value of these data through high quality gene expression curation and data integration, by providing bioinformatics tools optimized for Xenopus experiments, and by linking Xenopus data to other model organisms and to human data. Xenbase draws in data via pipelines that download data, parse the content, and save them into appropriate files and database tables. Furthermore, Xenbase makes these data accessible to the broader biomedical community by continually providing annotated data updates to organizations such as NCBI, UniProtKB and Ensembl. Here we describe our bioinformatics, genome-browsing tools, data acquisition and sharing, our community submitted and literature curation pipelines, text-mining support, gene page features and the curation of gene nomenclature and gene models.fga This article is protected by copyright. All rights reserved. © 2015 Wiley Periodicals, Inc.
    genesis 07/2015; 53(8). DOI:10.1002/dvg.22873