genesis (Genesis )

Publisher: John Wiley & Sons


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.

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  • Website
    Genesis website
  • Other titles
    Genesis (New York, N.Y.: 2000: Online), Genesis
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  • Material type
    Document, Periodical, Internet resource
  • Document type
    Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

John Wiley & Sons

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    • See Wiley-Blackwell entry for articles after February 2007
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    • 'John Wiley and Sons' is an imprint of 'Wiley-Blackwell'
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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: 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: LHX9 is a LIM-homeodomain transcription factor essential for the development of gonads, spinal cord interneurons, and thalamic neurons to name a few. We recently reported the expression of LHX9 in retinal amacrine cells during development. In this study, we generated an Lhx9 - GFPCreERT2 (GCE) knock-in mouse line by knocking-in a GCE cassette at the Lhx9 locus, thus inactivating endogenous Lhx9. Lhx9GCE/+ mice were viable, fertile, and displayed no overt phenotypical characteristics. Lhx9GCE/GCE mice were all phenotypically female, smaller in size, viable, but infertile. The specificity and efficacy of the Lhx9-GCE mouse line was verified by crossing it to a Rosa26 - tdTomato reporter mouse line, which reveals the Cre recombinase activities in retinal amacrine cells, developing limbs, testis, hippocampal neurons, thalamic neurons, and cerebellar neurons. Taken together, the Lhx9-GCE mouse line could serve as a beneficial tool for lineage tracing and gene manipulation experiments. © 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;
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    ABSTRACT: Neurod1 is a transcription factor involved in several developmental programs of the gastrointestinal tract, pancreas, neurosensory and central nervous system. In the brain, Neurod1 was shown to be essential for neurogenesis as well as migration, maturation and survival of newborn neurons during development and adulthood. Interestingly, Neurod1 is also expressed in a subset of fully mature neurons where its function remains unclear. To study the role of Neurod1, systems are required that allow the temporal and spatial genetic manipulation of Neurod1-expressing cells. To this aim we have generated four Neurod1-CreER(T2) mouse lines in which CreER(T2) expression, although at different levels, is restricted within areas of physiological Neurod1 expression and Neurod1 positive cells. In particular, the different levels of CreER(T2) expression in different mouse lines offers the opportunity to select the one that is more suited for a given experimental approach. Hence, our Neurod1-CreER(T2) lines provide valuable new tools for the manipulation of newborn neurons during development and adulthood as well as for studying the subpopulation of mature neurons that retain Neurod1 expression throughout life. In this context, we here report that Neurod1 is not only expressed in immature newborn neurons of the adult hippocampus, as already described, but also in fully mature granule cells of the dentate gyrus. © 2014 Wiley Periodicals, Inc.
    genesis 06/2014;
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    ABSTRACT: Transforming growth factor beta2 (TGFβ2) is a multifunctional protein which is expressed in several embryonic and adult organs. TGFB2 mutations can cause Loeys Dietz syndrome, and its dysregulation is involved in cardiovascular, skeletal, ocular and neuromuscular diseases, osteoarthritis, tissue fibrosis, and various forms of cancer. TGFβ2 is involved in cell growth, apoptosis, cell migration, cell differentiation, cell-matrix remodeling, epithelial-mesenchymal transition, and wound healing in a highly context-dependent and tissue-specific manner. Tgfb2-/- mice die perinatally from congenital heart disease, precluding functional studies in adults. Here, we have generated mice harboring Tgfb2βgeo (knockout-first lacZ-tagged insertion) gene-trap allele and Tgfb2flox conditional allele. Tgfb2βgeo/βgeo or Tgfb2βgeo/- mice died at perinatal stage from the same congenital heart defects as Tgfb2-/- mice. β-galactosidase staining successfully detected Tgfb2 expression in the heterozygous Tgfb2βgeo fetal tissue sections. Tgfb2flox mice were produced by crossing the Tgfb2+/βgeo mice with the FLPeR mice. Tgfb2flox/- mice were viable. Tgfb2 conditional knockout (Tgfb2cko/-) fetuses were generated by crossing of Tgfb2flox/- mice with Tgfb2+/-;EIIaCre mice. Systemic Tgfb2cko/- embryos developed cardiac defects which resembled the Tgfb2βgeo/βgeo, Tgfb2βgeo/-, and Tgfb2-/- fetuses. In conclusion, Tgfb2βgeo and Tgfb2flox mice are novel mouse strains which will be useful for investigating the tissue specific expression and function of TGFβ2 in embryonic development, adult organs, and disease pathogenesis and cancer. © 2014 Wiley Periodicals, Inc.
    genesis 06/2014;
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    ABSTRACT: This year marks the 125th anniversary of the beginning of regeneration research in the ascidian Ciona intestinalis. A brief note was published in 1891 reporting the regeneration of the Ciona neural complex and siphons. This launched an active period of Ciona regeneration research culminating in the demonstration of partial body regeneration: the ability of proximal body parts to regenerate distal ones, but not vice versa. In a process resembling regeneration, wounds in the siphon tube were discovered to result in the formation of an ectopic siphon. Ciona regeneration research then lapsed into a period of relative inactivity following the purported demonstration of the inheritance of acquired characters using siphon regeneration as a model. Around the turn of the present century, Ciona regeneration research experienced a new blossoming. The current studies established the morphological and physiological integrity of the regeneration process and its resemblance to ontogeny. They also determined some of the cell types responsible for tissue and organ replacement and their sources in the body. Finally, they showed that regenerative capacity is reduced with age. Many other aspects of regeneration now can be studied at the mechanistic level because of the extensive molecular tools available in Ciona. © 2014 Wiley Periodicals, Inc.
    genesis 06/2014;
  • genesis 06/2014; 52(6):451-4.
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    ABSTRACT: Fast and slow TnI are co-expressed in E11.5 embryos, and fast TnI is present from the very beginning of myogenesis. A novel green fluorescent protein (GFP) reporter mouse lines (FastTnI/GFP lines) that carry the primary and secondary enhancer elements of the mouse fast troponin I (fast TnI), in which reporter expression correlates precisely with distribution of the endogenous fTnI protein was generated. Using the FastTnI/GFP mouse model, we characterized the early myogenic events in mice, analyzing the migration of GFP-positive myoblasts, and the formation of primary and secondary myotubes in transgenic embryos. Interestingly, we found that the two contractile fast and slow isoforms of TnI are expressed during the migration of myoblasts from the somites to the limbs and body wall, suggesting that both participate in these events. Since no sarcomeres are present in myoblasts, we speculate that the function of fast TnI in early myogenesis is, like Myosin and Tropomyosin, to participate in cell movement during the initial myogenic stages. © 2014 Wiley Periodicals, Inc.
    genesis 06/2014;
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    ABSTRACT: The Drosophila Trithorax-like (Trl) gene encodes a GAGA factor which regulates a number of developmentally important genes. In this study, we identify a new function for Drosophila GAGA factor in male germ cell development. Trl mutants carrying strong hypomorphic alleles display loss of primordial germ cells during their migration in embryogenesis and severe disruption in mitochondria structure during early spermatogenesis. The mutation resulted in small testes formation, a deficit of germ cells, abnormal mitochondrial morphogenesis, spermatocyte death through autophagy and partial or complete male sterility. Pleiotropic mutation effects can be explained by the misexpression of GAGA factor target genes, the products of which are required for germ cell progression into mature sperm. © 2014 Wiley Periodicals, Inc.
    genesis 05/2014;
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    ABSTRACT: Genes required for an organism to develop to maturity (for which no other gene can compensate) are considered essential. The continuing functional annotation of the mouse genome has enabled the identification of many essential genes required for specific developmental processes including cardiac development. Patterns are now emerging regarding the functional nature of genes required at specific points throughout gestation. Essential genes required for development beyond cardiac progenitor cell migration and induction include a small and functionally homogenous group encoding transcription factors, ligands and receptors. Actions of core cardiogenic transcription factors from the Gata, Nkx, Mef, Hand and Tbx families trigger a marked expansion in the functional diversity of essential genes from mid-gestation onwards. As the embryo grows in size and complexity, genes required to maintain a functional heartbeat and to provide muscular strength and regulate blood flow are well represented. These essential genes regulate further specialisation and polarisation of cell types along with proliferative, migratory, adhesive, contractile and structural processes. The identification of patterns regarding the functional nature of essential genes across numerous developmental systems may aid prediction of further essential genes and those important to development and/or progression of disease. © 2014 Wiley Periodicals, Inc.
    genesis 05/2014;
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    ABSTRACT: Notch signaling is important in angiogenesis during embryonic development. However, the embryonic lethal phenotypes of knock-out and transgenic mice have precluded studies of the role of Notch post-natally. To develop a mouse model that would bypass the embryonic lethal phenotype and investigate the possible role of Notch signaling in adult vessel growth, we developed transgenic mice with Cre-conditional expression of the constitutively active intracellular domain of Notch1 (IC-Notch1). Double transgenic IC-Notch1/Tie2-Cre embryos with endothelial specific IC-Notch1 expression died at embryonic day 9.5. They displayed collapsed and leaky blood vessels and defects in angiogenesis development. A tetracycline-inducible system was used to express Cre recombinase postnatally in endothelial cells. In adult mice IC-Notch1 expression inhibited bFGF-induced neovascularization and female mice lacked mature ovarian follicles, which may reflect the block in bFGF-induced angiogenesis required for follicle growth. Our results demonstrate that Notch signaling is important for both embryonic and adult angiogenesis and indicate that the Notch signaling pathway may be a useful target for angiogenic therapies. © 2014 Wiley Periodicals, Inc.
    genesis 05/2014;

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