Developmental Dynamics (DEV DYNAM)

Publisher: American Association of Anatomists, Wiley

Journal description

Developmental Dynamics an official publication of the American Association of Anatomists provides a focus for communication among developmental biologists who study the emergence of form during animal development. The journal is an international forum for the exchange of novel and significant information gained from analytical and theoretical investigations on the mechanisms that control morphogenesis. Developmental Dynamics seeks manuscripts on work done at all levels of biological organization ranging from the molecular to the organismal. Representative topics of Interest Include: Mechanisms underlying morphogenesis Pattern formation Tissue organization and repair Transcriptional and post-transcriptional controls governing the emergence of diverse biologic form Analytical methods for the visualization of molecular cytologic and ultrastructural aspects of dynamic developmental processes Cell-cell signalling and cell-matrix interactions Genetic and molecular probes for the study of cell lineages and developmental pathways Transgenic approaches for studying the control of tissue- and organ-specific gene expression Mathematical models of morphogenetic processes.

Current impact factor: 2.38

Impact Factor Rankings

2016 Impact Factor Available summer 2017
2014 / 2015 Impact Factor 2.376
2013 Impact Factor 2.668
2012 Impact Factor 2.59
2011 Impact Factor 2.536
2010 Impact Factor 2.864
2009 Impact Factor 2.833
2008 Impact Factor 3.018
2007 Impact Factor 3.084
2006 Impact Factor 3.169
2005 Impact Factor 3.333
2004 Impact Factor 2.868
2003 Impact Factor 3.16
2002 Impact Factor 3.804
2001 Impact Factor 3.485
2000 Impact Factor 3.131
1999 Impact Factor 3.939
1998 Impact Factor 3.244
1997 Impact Factor 3.624
1996 Impact Factor 3.784
1995 Impact Factor 3.183
1994 Impact Factor 2.483
1993 Impact Factor 1.433

Impact factor over time

Impact factor

Additional details

5-year impact 2.53
Cited half-life 8.40
Immediacy index 0.62
Eigenfactor 0.02
Article influence 1.04
Website Developmental Dynamics website
Other titles Developmental dynamics
ISSN 1058-8388
OCLC 24403911
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

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

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: In Ts65Dn, a mouse model of Down syndrome (DS), brain and craniofacial abnormalities that parallel those in people with DS are linked to an attenuated cellular response to sonic hedgehog (SHH) signaling. If a similarly reduced response to SHH occurs in all trisomic cells, then chronic up-regulation of the pathway might have a positive effect on development in trisomic mice, resulting in amelioration of the craniofacial anomalies. Results: We crossed Ts65Dn with Ptch1(tm1Mps/+) mice and quantified the craniofacial morphology of Ts65Dn;Ptch(+/-) offspring to assess whether a chronic up-regulation of the SHH pathway rescued DS-related anomalies. Ts65Dn;Ptch1(+/-) mice experience a chronic increase in SHH in SHH-receptive cells due to haploinsufficiency of the pathway suppressor, Ptch1. Chronic up-regulation had minimal effect on craniofacial shape and did not correct facial abnormalities in Ts65Dn;Ptch(+/-) mice. We further compared effects of this chronic up-regulation of SHH to acute pathway stimulation in mice treated on the day of birth with a SHH pathway agonist, SAG. We found that SHH affects facial morphology differently based on chronic vs. acute postnatal pathway up-regulation. Conclusions: Our findings have implications for understanding the function of SHH in craniofacial development and for the potential use of SHH-based agonists to treat DS-related abnormalities. This article is protected by copyright. All rights reserved.
    No preview · Article · Oct 2015 · Developmental Dynamics
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    ABSTRACT: Background: During the course of development, the vertebrate nephric duct (ND) extends and migrates from the place of its initial formation, adjacent to the anterior somites, until it inserts into the bladder or cloaca in the posterior region of the embryo. The molecular mechanisms that guide ND migration are poorly understood. Results: A novel Gata3-enhancer-Gfp-based chick embryo live imaging system was developed which permits documentation of ND migration at the individual cell level for the first time. FGF Receptors and FGF response genes are expressed in the ND, FGF ligands are expressed in surrounding tissues. FGF receptor inhibition blocked nephric duct migration. Individual inhibitors of the Erk, p38, or Jnk pathways did not affect duct migration, but inhibition of all three pathways together did inhibit migration of the duct. A localized source of FGF8 placed adjacent to the nephric duct did not affect the duct migration path. Conclusions: FGF signaling acts as a "motor" that is required for duct migration, but other signals are needed to determine the directionality of the duct migration pathway. This article is protected by copyright. All rights reserved. © 2014 Wiley Periodicals, Inc.
    No preview · Article · Feb 2015 · Developmental Dynamics
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    ABSTRACT: Background: Congenital loss of the SHOX gene is considered to be a genetic cause of short stature phenotype in Turner syndrome and Leri-Weill dyschondrosteosis patients. Though SHOX expression initiates during early fetal development, little is known about the embryonic roles of SHOX. The evolutionary conservation of the zebrafish shox gene and the convenience of the early developmental stages for analyses make zebrafish a preferred model. Here, we characterized structure, expression, and developmental roles of zebrafish shox through a loss of function approach. Results: We found a previously undiscovered Shox protein that has both a homeodomain and an OAR-domain in zebrafish. The shox transcript emerged during the segmentation period and it increased in later stages. The predominant domains of shox expression were mandibular arch, pectoral fin, anterior notochord, rhombencephalon and mesencephalon, suggesting that Shox is involved in bone and neural development. Translational blockade of Shox mRNA by an antisense morpholino oligo delayed embryonic growth, which was restored by the co-overexpression of morpholino-resistant Shox mRNA. At later stages, impaired Shox expression markedly delayed the calcification process in the anterior vertebral column and craniofacial bones. Conclusions: Our data demonstrate evolutionarily-conserved Shox plays roles in early embryonic growth and in later bone formation. This article is protected by copyright. All rights reserved. ©2014. Wiley Periodicals, Inc.
    No preview · Article · Feb 2015 · Developmental Dynamics
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    ABSTRACT: Endothelial-mesenchymal transformation (EndMT) is essential for endocardial cushion formation during cardiac morphogenesis. We recently identified Tmem100 as an endothelial gene indispensable for vascular development. In this study, we further investigated its roles for EndMT during atrioventricular canal (AVC) cushion formation. Tmem100 was expressed in AVC endocardial cells, and Tmem100 null embryos showed severe EndMT defect in the AVC cushions. While calcineurin-dependent suppression of vascular endothelial growth factor (VEGF) expression in the AVC myocardium is important for EndMT, significant up-regulation of Vegfa expression was observed in Tmem100 null heart. EndMT impaired in Tmem100 null AVC explants was partially but significantly restored by the expression of constitutively-active calcineurin A, suggesting dysregulation of myocardial calcineurin-VEGF signaling in Tmem100 null heart. Moreover, Tmem100 null endocardial cells in explant culture did not show EndMT in response to the treatment with myocardium-derived growth factors, transforming growth factor β2 and bone morphogenetic protein 2, indicating involvement of an additional endocardial-specific abnormality in the mechanism of EndMT defect. The lack of NFATc1 nuclear translocation in endocardial cells of Tmem100 null embryos suggests impairment of endocardial calcium signaling. The Tmem100 deficiency causes EndMT defect during AVC cushion formation possibly via disturbance of multiple calcium-related signaling events. Developmental Dynamics 244:31-42, 2015. © 2014 Wiley Periodicals, Inc. © 2014 Wiley Periodicals, Inc.
    No preview · Article · Jan 2015 · Developmental Dynamics
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    ABSTRACT: The tumor suppressor protein merlin is thought to regulate cell proliferation and cell adhesion through interaction with protein partners. Loss of merlin is associated with Neurofibromatosis Type 2 (NF2) tumors. NHERF1 or EBP50 is a scaffolding protein that functions in apical organization of polarized cells. Merlin and NHERF1 have been shown to interact in vitro in vertebrates. We investigate how the Drosophila NHERF1 orthologue, Sip1, and Merlin function to regulate cell proliferation and adhesion. We identify two conserved arginine residues (R325 and R335) in Merlin which, in addition to the FERM domain, are required for interaction with Sip1. Mutation of the arginine residues result in reduced Sip1 binding to Merlin and loss of Merlin growth suppressor function. Over-expression of Merlin(R325A) and/or Merlin(R335L) in Drosophila wings result in increased proliferation in the adult wing (increase in size), which is rescued by co-over-expression of constitutively active Merlin protein. Reduced Sip1 binding to Merlin also produces defects in adhesion in follicle epithelial cells. Sip1 facilitates the activation of Merlin as a tumor suppressor protein. Thus, our work provides insight into how Merlin functions as a tumor suppressor and in adhesion and this provides insight into the mechanism of NF2 pathogenesis. Developmental Dynamics 243:1554-1570, 2014. © 2014 Wiley Periodicals, Inc. © 2014 Wiley Periodicals, Inc.
    No preview · Article · Dec 2014 · Developmental Dynamics
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    ABSTRACT: The zebrafish heart regenerates after various severe injuries. Common processes of heart regeneration are cardiomyocyte proliferation, activation of epicardial tissue, and neovascularization. In order to further characterize heart regeneration processes, we introduced milder injuries and compared responses to those induced by ventricular apex resection, a widely used injury method. We used scratching of the ventricular surface and puncturing of the ventricle with a fine tungsten needle as injury-inducing techniques.
    Preview · Article · Nov 2014 · Developmental Dynamics
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    No preview · Article · Aug 2014 · Developmental Dynamics
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    ABSTRACT: BACKGROUND: Planarians are renowned for their capacity to replace lost tissues from adult pluripotent stem cells (neoblasts). Here we report that Lissencephaly-1 (lis1), which has roles in cellular processes such as mitotic spindle apparatus orientation and in signal regulation required for stem cell self-renewal, is required for stem cell maintenance in the planarian Schmidtea mediterranea. RESULTS: In planarians, lis1 is expressed in differentiated tissues and stem cells. lis1 RNAi leads to head regression, ventral curling, and death by lysis. By labeling the neoblasts and proliferating cells, we found lis1 knockdown animals show a dramatic increase in the number of mitotic cells, followed by depletion of the stem cell pool. Analysis of the mitotic spindles in dividing neoblasts revealed that defective spindle positioning is correlated with cells arrested at metaphase. In addition, we show that inhibiting a planarian homologue of nudE, predicted to encode a LIS-1 interacting protein, also leads to cell cycle progression defects. CONCLUSIONS: Our results provide evidence for a conserved role of LIS1 and NUDE in regulating the function of the mitotic spindle apparatus in a representative Lophotrochozoan and that planarians will be useful organisms in which to investigate LIS1 regulation of signaling events underlying stem cell self-renewal.
    No preview · Article · May 2012 · Developmental Dynamics

  • No preview · Article · Jan 2010 · Developmental Dynamics