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
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    • 12 months embargo
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    • On author's personal website, institutional repositories, arXiv, AgEcon, PhilPapers, PubMed Central, RePEc or Social Science Research Network
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    • Author's pre-print must acknowledge acceptance for publication
    • Non-Commercial
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    • 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

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Gene trapping has emerged as a valuable tool to create conditional alleles in various model organisms. Here we report the FLEx-based gene trap vector SAGFLEx that allows the generation of conditional mutations in zebrafish by gene-trap mutagenesis. The SAGFLEx gene trap cassette comprises the rabbit β-globin splice acceptor and the coding sequence of GFP, flanked by pairs of inversely oriented heterotypic target sites for the site-specific recombinases Cre and Flp. Insertion of the gene-trap cassette into endogenous genes can result in conditional mutations that are stably inverted by Cre and Flp, respectively. To test the functionality of this system we performed a pilot screen and analyzed the insertion of the gene-trap cassette into the lima1a gene locus. In this lima1a allele, GFP expression faithfully recapitulated the endogenous lima1a expression and resulted in a complete knockout of the gene in homozygosity. Application of either Cre or Flp was able to mediate the stable inversion of the gene trap cassette and showed the ability to conditionally rescue or reintroduce the gene inactivation. Combined with pharmacologically inducible site specific recombinases the SAGFLEx vector insertions will enable precise conditional knockout studies in a spatial- and temporal-controlled manner. This article is protected by copyright. All rights reserved.
    genesis 11/2015; DOI:10.1002/dvg.22909
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    ABSTRACT: The kappa opioid receptor (KOR) has numerous important roles in the nervous system including the modulation of mood, reward, pain, and itch. In addition, KOR is expressed in many non-neuronal tissues. However, the specific cell types that express KOR are poorly characterized. Here, we report the development of a KOR-Cre knockin allele, which provides genetic access to cells that express KOR. In this mouse, Cre recombinase (Cre) replaces the initial coding sequence of the Opkr1 gene (encoding the kappa opioid receptor). We demonstrate that the KOR-Cre allele mediates recombination by embryonic day 14.5 (E14.5). Within the brain, KOR-Cre shows expression in numerous areas including the cerebral cortex, nucleus accumbens and striatum. In addition, this allele is expressed in epithelium and throughout many regions of the body including the heart, lung, and liver. Finally, we reveal that KOR-Cre mediates recombination of a subset of bipolar and amacrine cells in the retina. Thus, the KOR-Cre mouse line is a valuable new tool for conditional gene manipulation to enable the study of KOR. This article is protected by copyright. All rights reserved.
    genesis 11/2015; DOI:10.1002/dvg.22910
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    ABSTRACT: Zebrafish with defective Nodal signaling have a phenotype analogous to the fatal human birth defect anencephaly, which is caused by an open anterior neural tube. Previous work in our laboratory found that anterior open neural tube defects in Nodal signaling mutants were caused by defects in mesendodermal/mesodermal tissue. Defects in these mutants are already apparent at neural plate stage, before the neuroepithelium starts to fold into a tube. Consistent with this, we found that the requirement for Nodal signaling maps to mid-late blastula stages. This timing correlates with the timing of prechordal plate mesendoderm and anterior mesoderm induction, suggesting these tissues act to promote neurulation. To further identify tissues important for neurulation, we took advantage of the variable phenotypes in Nodal signaling-deficient sqt mutant and Lefty1-overexpressing embryos. Statistical analysis indicated a strong, positive correlation between a closed neural tube and presence of several mesendoderm/mesoderm-derived tissues (hatching glands, cephalic paraxial mesoderm, notochord, and head muscles). However, the neural tube was closed in a subset of embryos that lacked any one of these tissues. This suggests that several types of Nodal-induced mesendodermal/mesodermal precursors are competent to promote neurulation. This article is protected by copyright. All rights reserved.
    genesis 11/2015; DOI:10.1002/dvg.22908
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    ABSTRACT: Porcine trophoblast-derived stem-like cells grown into serum medium start to differentiate and become senescent within 30 days. However, trophoblast derived cells, cultured in vitro in a defined and non-serum medium, have the regenerative properties, such as indefinite passage, and foreign DNA receptivity, similar to stem cells. To evaluate the biochemical, biophysical and genetic changes of the terminal differentiation of trophoblast derived cells, Raman microspectroscopy, atomic force microscopy and qPCR were applied. It was found that Raman spectral intensities of characteristic peaks, cell morphology, and Young's modulus can be used to distinguish differentiated and undifferentiated trophoblast cells. In addition, 17 cytoskeleton and extracellular matrix-related genes were significantly impacted by medium type (non-serum versus serum). Our findings suggest that Raman microspectroscopy and atomic force microscopy - both considered as label-free, non-invasive techniques-can be applied to distinguish differentiated trophoblast cells, and cellular biochemical information and biophysical properties can be indicative of cellular differences during cell differentiation. In addition, most of cytoskeleton-related genes exhibit similar pattern to that of Young's modulus during trophoblast cell differentiation, indicating the potential connection between cytoskeleton-related genes and cellular stiffness. This article is protected by copyright. All rights reserved.
    genesis 10/2015; DOI:10.1002/dvg.22907
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    ABSTRACT: Misexpression Suppressor of Ras 4 (MESR4), a plant homeodomain (PHD) finger protein with nine zinc-finger motifs has been implicated in various biological processes including the regulation of fat storage and innate immunity in Drosophila. However, the role of MESR4 in the context of development remains unclear. Here we show that MESR4 is a nuclear protein essential for embryonic development. Immunostaining of polytene chromosomes using anti-MESR4 antibody revealed that MESR4 binds to numerous bands along the chromosome arms. The most intense signal was detected at the 39E-F region, which is known to contain the histone gene cluster. We identified P-element insertions in the MESR4 locus, which were homozygous lethal during embryogenesis with defects in ventral ectoderm formation and head encapsulation. In the mutant embryos, expression of Fasciclin 3 (Fas3), an EGFR signal target gene was greatly reduced, and the level of EGFR signal-dependent double phosphorylated ERK (dp-ERK) remained low. However, in the context of wing vein formation, genetic interaction experiments suggested that MESR4 is involved in the EGFR signaling as a negative regulator. These results suggest that MESR4 is a novel chromatin-binding protein required for proper expression of genes including those regulated by the EGFR signaling pathway during development. This article is protected by copyright. All rights reserved.
    genesis 10/2015; DOI:10.1002/dvg.22906
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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 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; 53(10). 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; 53(10). 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; 53(9). 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