genesis (Genesis )

Publisher: John Wiley & Sons

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.

  • Impact factor
    2.58
  • 5-year impact
    2.73
  • Cited half-life
    8.10
  • Immediacy index
    0.55
  • Eigenfactor
    0.01
  • Article influence
    1.40
  • 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

John Wiley & Sons

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • See Wiley-Blackwell entry for articles after February 2007
    • On personal web site or secure external website at authors institution
    • Not allowed on institutional repository
    • JASIST authors may deposit in an institutional repository
    • Non-commercial
    • Pre-print must be accompanied with set phrase (see individual journal copyright transfer agreements)
    • Published source must be acknowledged with set phrase (see individual journal copyright transfer agreements)
    • Publisher's version/PDF cannot be used
    • Articles in some journals can be made Open Access on payment of additional charge
    • 'John Wiley and Sons' is an imprint of 'Wiley-Blackwell'
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Rearrangements in the Sxr-region include Sry coding sequences, are a likely by-product of secondary structure formation and are genetically modulated. Submitted and accepted by Genesis pending revisions. Under revision.
    genesis 01/2015; Under revision.
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    ABSTRACT: As a group closely related to chordates, hemichordate acorn worms are in a key phylogenic position for addressing hypotheses of chordate origins. The stomochord of acorn worms is an anterior outgrowth of the pharynx endoderm into the proboscis. In 1886 Bateson proposed homology of this organ to the chordate notochord, crowning this animal group "hemichordates". Although this proposal has been debated for over a century, the question still remains unresolved. Here we review recent progress related to this question. First, the developmental mode of the stomochord completely differs from that of the notochord. Second, comparison of expression profiles of genes including Brachyury, a key regulator of notochord formation in chordates, does not support the stomochord/notochord homology. Third, FoxE that is expressed in the stomochord-forming region in acorn worm juveniles is expressed in the club-shaped gland and in the endostyle of amphioxus, in the endostyle of ascidians, and in the thyroid gland of vertebrates. Based on these findings, together with the anterior endodermal location of the stomochord, we propose that the stomochord has evolutionary relatedness to chordate organs deriving from the anterior pharynx rather than to the notochord. © 2014 Wiley Periodicals, Inc.
    genesis 10/2014;
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    ABSTRACT: The spleen is a lymphoid organ that serves as a unique niche for immune reactions, extramedullary hematopoiesis, and the removal of aged erythrocytes form the circulation. While much is known about the immunological functions of the spleen, the mechanisms governing the development and organization of its stromal microenvironment remain poorly understood. Here we report the generation and analysis of a Tlx1CreER-Venus knock-in mouse strain engineered to simultaneously express tamoxifen-inducible CreERT2 and Venus fluorescent protein under the control of regulatory elements of the Tlx1 gene, which encodes a transcription factor essential for spleen development. We demonstrated that Venus as well as CreER expression recapitulates endogenous Tlx1 transcription within the spleen microenvironment. When Tlx1CreER-Venus mice were crossed with the Cre-inducible reporter strain, Tlx1-expressing cells as well as their descendants were specifically labelled following tamoxifen administration. We also showed by cell lineage tracing that asplenia caused by Tlx1 deficiency is attributable to altered contribution of mesenchymal cells in the spleen anlage to the pancreatic mesenchyme. Thus, Tlx1CreER-Venus mice represent a new tool for lineage tracing and conditional gene manipulation of spleen mesenchymal cells, essential approaches for understanding the molecular mechanisms of spleen development. © 2014 Wiley Periodicals, Inc.
    genesis 10/2014;
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    ABSTRACT: Transgenic mice were generated using a heat shock protein 2 (Hspa2) gene promoter to express green fluorescent protein (GFP) at the beginning of meiotic prophase I in spermatocytes. Expression was confirmed in four lines by in situ fluorescence, immunohistochemistry, western blotting, and PCR assays. The expression and distribution of the GFP and HSPA2 proteins co-localized in spermatocytes and spermatids in three lines, but GFP expression was variegated in one line (F46), being present in some clones of meiotic and post-meiotic germ cells and not in others. Fluorescence-activated cell-sorting (FACS) was used to isolate purified populations of spermatocytes and spermatids. Although bisulfite sequencing revealed differences in the DNA methylation patterns in the promoter regions of the transgene of the variegated expressing GFP line, a uniformly expressing GFP reporter line, and the Hspa2 gene, these differences did not correlate with variegated expression. The Hspa2-GFP reporter mice provide a novel tool for studies of meiosis by allowing detection of GFP in situ and in isolated spermatogenic cells. They will allow sorting of meiotic and post-meiotic germ cells for characterization of molecular features and correlation of expression of GFP with stage-specific spermatogenic cell proteins and developmental events. © 2014 Wiley Periodicals, Inc.
    genesis 10/2014;
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    ABSTRACT: Tunicates are invertebrate members of the chordate phylum, and are considered to be the sister group of vertebrates. Tunicates are composed of ascidians, thaliaceans and appendicularians. With the advent of inexpensive high throughput sequencing, the number of sequenced tunicate genomes is expected to rise sharply within the coming years. To facilitate comparative genomics within the tunicates, and between tunicates and vertebrates, standardized rules for the nomenclature of tunicate genetic elements need to be established. Here we propose a set of nomenclature rules, consensual within the community, for predicted genes, pseudogenes, transcripts, operons, transcriptional cis-regulatory regions, transposable elements, and transgenic constructs. In addition, the document proposes guidelines for naming transgenic and mutant lines. The latest version of these guidelines can be downloaded from the Tunicate Portal (http://www.tunicate-portal.org/). To better identify the latest version, the file name for the guidelines should follow the following syntax: Genetic_Guidelines_Tunicate_[year]_[month]_[day] (example, Genetic_Guidelines_Tunicate_2014_05_01). © 2014 Wiley Periodicals, Inc.
    genesis 09/2014;
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    ABSTRACT: Chromatin remodeling via incorporation of histone variants plays a key role in the regulation of embryonic development. The histone variant H3.3 has been associated with a number of early events including formation of the paternal pronucleus upon fertilization. The small number of amino acid differences between H3.3 and its canonical counterparts (H3.1 and H3.2) has limited studies of the developmental significance of H3.3 deposition into chromatin due to difficulties in distinguishing the H3 isoforms. To this end, we used zinc-finger nuclease (ZFN) mediated gene editing to introduce a small C-terminal hemagglutinin (HA) tag to the endogenous H3.3B locus in mouse embryonic stem cells (ESCs), along with an internal ribosome entry site (IRES) and a separately translated fluorescent reporter of expression. This system will allow detection of expression driven by the reporter in cells, animals, and embryos, and will facilitate investigation of differential roles of paternal and maternal H3.3 protein during embryogenesis that would not be possible using variant-specific antibodies. Further, the ability to monitor endogenous H3.3 protein in various cell lineages will enhance our understanding of the dynamics of this histone variant over the course of development. © 2014 Wiley Periodicals, Inc.
    genesis 09/2014;
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    ABSTRACT: Homologous recombination in embryonic stem cells (ESCs) is widely utilized in genome engineering, particularly in the generation of gene targeted mice. However, genome engineering is often plagued by the problem of low homologous recombination efficiency. In this study, we developed a novel method to increase the efficiency of homologous recombination in ESCs by changing its culture conditions. By comparing the efficiency of different ESCs in various culture conditions, we determined that chemicals that inhibit the MEK and GSK3β pathways (2i condition) enhance homologous recombination and eliminate differences in efficiencies among cell lines. Analysis of gene expression patterns in ESCs maintained in different culture conditions has identified several homologous recombination-related candidates, including the pluripotent markers Eras and Tbx3. The results of this study suggest that homologous recombination is associated with ESC pluripotency. © 2014 Wiley Periodicals, Inc.
    genesis 09/2014;
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    ABSTRACT: The phox2b gene encodes a transcription factor that is expressed in the developing enteric nervous system (ENS). An enhancer element has been identified in the zebrafish phox2b locus that can drive tissue specific expression of reporter genes in enteric neuron precursor cells. We have generated a transgenic zebrafish line in which the Kaede fluorescent protein is under the control of this phox2b enhancer. This line has stable expression of the Kaede protein in enteric neuron precursor cells over 3 generations. To demonstrate the utility of this line we compared the migration and division rates of enteric neuron precursor cells in wild type and the zebrafish ENS mutant lessen. © 2014 Wiley Periodicals, Inc.
    genesis 09/2014;
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    ABSTRACT: Focal Adhesion Kinase is a non-receptor protein tyrosine kinase with signalling functions downstream of integrins and growth factor receptors. In addition to its role in adhesion, migration and proliferation it also has non-kinase scaffolding functions in the nucleus. FAK activation involves the following: (1) ligand bound growth factors or clustered integrins activate FAK kinase domain; (2) FAK autophosphorylates Tyrosine (Y) 397; (3) Src binds pY397 and phosphorylates FAK at various other sites including Y861; (4) downstream signalling of activated FAK elicits changes in cellular behaviour. Although many studies have demonstrated roles for the kinase domain, Y397 and Y861 sites in vitro much less is known about their functions in vivo. Here we report the generation of a series of FAK-mutant knockin mice where mutant FAK, either kinase dead (KD), non-phosphorylatable mutants Y397F and Y861F or mutant Y397E – containing a phosphomimetic site that results in a constitutive active Y397, can be expressed in a Cre inducible fashion driven by the ROSA26 promoter. In future studies, intercrossing these mice with FAKflox/flox mice and inducible cre-expressing mice will enable the in vivo study of mutant FAK function in the absence of endogenous FAK in a spatially and temporally regulated fashion within the whole organism. © 2014 Wiley Periodicals, Inc.
    genesis 09/2014;
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    ABSTRACT: Botryllus schlosseri is a colonial ascidian with characteristics that make it an attractive model for studying immunology, stem cell biology, evolutionary biology, and regeneration. Transcriptome sequencing and the recent completion of a draft genome sequence for B. schlosseri have revealed a large number of genes, both with and without vertebrate homologs, but analyzing the spatial and temporal expression of these genes in situ has remained a challenge. Here we report a robust protocol for in situ hybridization that enables the simultaneous detection of multiple transcripts in whole adult B. schlosseri using Tyramide Signal Amplification in conjunction with digoxigenin- and dinitrophenol-labeled RNA probes. Using this protocol we have identified a number of genes that can serve as markers for developing and mature structures in B. schlosseri, permitting analysis of phenotypes induced in loss-of-function experiments. © 2014 Wiley Periodicals, Inc.
    genesis 09/2014;
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    ABSTRACT: Developmental biology relies heavily on microscopy to image the finely-controlled cell behaviors that drive embryonic development. Most embryos are large enough that a field of view with the resolution and magnification needed to resolve single cells will not span more than a small region of the embryo. Ascidian embryos, however, are sufficiently small that they can be imaged in toto with fine subcellular detail using conventional microscopes and objectives. Unlike other model organisms with particularly small embryos, ascidians have a chordate embryonic body plan that includes a notochord, hollow dorsal neural tube, heart primordium and numerous other anatomical details conserved with the vertebrates. Here we compare the size and anatomy of ascidian embryos with those of more traditional model organisms, and relate these features to the capabilities of both conventional and exotic imaging methods. We review the emergence of Ciona and related ascidian species as model organisms for a new era of image-based developmental systems biology. We conclude by discussing some important challenges in ascidian imaging and image analysis that remain to be solved. © 2014 Wiley Periodicals, Inc.
    genesis 09/2014;
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    ABSTRACT: The Hairy-related transcription factor family of Notch- and ALK1-downstream transcriptional repressors, called Hrt/Hey/Hesr/Chf/Herp/Gridlock, has complementary and indispensable functions for vascular development. While mouse embryos null for either Hrt1/Hey1 or Hrt2/Hey2 did not show early vascular phenotypes, Hrt1/Hey1; Hrt2/Hey2 double null mice (H1ko/H2ko) showed embryonic lethality with severe impairment of vascular morphogenesis. It remained unclear, however, whether Hrt/Hey functions are required in endothelial cells or vascular smooth muscle cells. In this study, we demonstrate that mice with endothelial-specific deletion of Hrt2/Hey2 combined with global Hrt1/Hey1 deletion (H1ko/H2eko) show abnormal vascular morphogenesis and embryonic lethality. Their defects were characterized by the failure of vascular network formation in the yolk sac, abnormalities of embryonic vascular structures and impaired smooth muscle cell recruitment, and were virtually identical to the H1ko/H2ko phenotypes. Among signaling molecules implicated in vascular development, Robo4 expression was significantly increased and activation of Src family kinases was suppressed in endothelial cells of H1ko/H2eko embryos. The present study indicates an important role of Hrt1/Hey1 and Hrt2/Hey2 in endothelial cells during early vascular development, and further suggests involvement of Robo4 and Src family kinases in the mechanisms of embryonic vascular defects caused by the Hrt/Hey deficiency. © 2014 Wiley Periodicals, Inc.
    genesis 09/2014;
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    ABSTRACT: Embryonic and post-embryonic development in ascidians have been studied for over a century, but it is only in the last 10 years that the complex molecular network involved in coordinating post-larval development and metamorphosis has started to emerge. In most ascidians, the transition from the larval to the sessile juvenile/adult, or metamorphosis, requires a combination of environmental and endogenous signals and is characterized by coordinated global morphogenetic changes that are initiated by the adhesion of the larvae. Cloney was the first to describe cellular events of ascidians' metamorphosis in 1978 and only recently elements of the molecular regulation of this crucial developmental step have been revealed. This review aims to present a thorough view of this crucial developmental step by combining recent molecular data to the already established cellular events. © 2014 Wiley Periodicals, Inc.
    genesis 09/2014;
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    ABSTRACT: We describe a novel zebrafish line that fluorescently tags a previously unknown protein, CT74a, allowing us to follow its endogenous expression in real time and at subcellular resolution in live embryos. Our results showed that CT74a-Citrine fusion protein is expressed in the developing pharyngeal arches, hindbrain, and fin buds in a pattern highly reminiscent of transcription factors belonging to anterior Hox gene families, including expression in a subset of neuronal nuclei. Consistent with this, splinkerette-PCR revealed that CT74a-Citrine’s genomic integration is within the HoxB region, and 3’ RACE demonstrated that its downstream coding sequence has no recognizable homology. Thus, CT74a is a previously unknown protein located within the HoxB cluster adjacent to Hoxb4a and is expressed in a Hoxb4a-like pattern. © 2014 Wiley Periodicals, Inc.
    genesis 08/2014;
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    ABSTRACT: The molecular events that control cell fate determination in cardiac and smooth muscle lineages remain elusive. Myocardin is an important transcription co-factor that regulates cell proliferation, differentiation and development of the cardiovascular system. Here, we describe the construction and analysis of a dual Cre and Enhanced Green Fluorescent Protein (EGFP) knock-in mouse line in the Myocardin locus (MyocdKI). We report that the MyocdKI allele expresses the Cre enzyme and the EGFP in a manner that recapitulates endogenous Myocardin expression patterns. We show that Myocardin expression marks the earliest cardiac and smooth muscle lineages. Furthermore, this genetic model allows for the identification of a cardiac cell population which maintains both Myocardin and Isl-1 expression, in E7.75 - E8.0 embryos, highlighting the contributions and merge of the first and second heart fields during cardiogenesis. Therefore, the MyocdKI allele is a unique tool for studying cardiovascular development and lineage-specific gene manipulation. © 2014 Wiley Periodicals, Inc.
    genesis 08/2014;
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    ABSTRACT: Glial cells missing (Gcm) is the primary regulator of glial cell fate in Drosophila. Gcm belongs to a small family of transcriptional regulators involved in fundamental developmental processes found in diverse animal phyla including vertebrates. Gcm proteins contain the highly conserved DNA-binding GCM domain, which recognizes an octamer DNA sequence. To date, studies in Drosophila have primarily relied on gcm alleles caused by P-element induced DNA deletions at the gcm locus, as well as a null allele caused by a single base pair substitution in the GCM domain that completely abolishes DNA binding. Here I characterize two hypomorphic missense alleles of gcm with intermediate glial cells missing phenotypes. In embryos homozygous for either of these gcm alleles the number of glial cells in the central nervous cystem (CNS) is reduced approximately in half. Both alleles have single amino acid changes in the GCM domain. These results suggest that Gcm protein activities in these mutant alleles have been attenuated such that they are operating at threshold levels, and trigger glial cell differentiation neural precursors in the CNS in a stochastic fashion. These hypomorphic alleles provide additional genetic resources for understanding Gcm functions and structure in Drosophila and other species. © 2014 Wiley Periodicals, Inc.
    genesis 07/2014;