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Journal Cover Journal of Developmental Biology
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  This is an Open Access Journal Open Access journal
   ISSN (Online) 2221-3759
   Published by MDPI Homepage  [140 journals]
  • JDB, Vol. 4, Pages 13: Hoxa5: A Key Player in Development and Disease

    • Authors: Lucie Jeannotte, Florian Gotti, Kim Landry-Truchon
      First page: 13
      Abstract: A critical position in the developmental hierarchy is occupied by the Hox genes, which encode transcription factors. Hox genes are crucial in specifying regional identity along the embryonic axes and in regulating morphogenesis. In mouse, targeted mutations of Hox genes cause skeletal transformations and organ defects that can impair viability. Here, we present the current knowledge about the Hoxa5 gene, a paradigm for the function and the regulation of Hox genes. The phenotypic survey of Hoxa5−/− mice has unveiled its critical role in the regional specification of the skeleton and in organogenesis. Most Hoxa5−/− mice die at birth from respiratory distress due to tracheal and lung dysmorphogenesis and impaired diaphragm innervation. The severity of the phenotype establishes that Hoxa5 plays a predominant role in lung organogenesis versus other Hox genes. Hoxa5 also governs digestive tract morphogenesis, thyroid and mammary glands development, and ovary homeostasis. Deregulated Hoxa5 expression is reported in cancers, indicating Hoxa5 involvement in tumor predisposition and progression. The dynamic Hoxa5 expression profile is under the transcriptional control of multiple cis-acting sequences and trans-acting regulators. It is also modulated by epigenetic mechanisms, implicating chromatin modifications and microRNAs. Finally, lncRNAs originating from alternative splicing and distal promoters encompass the Hoxa5 locus.
      PubDate: 2016-03-25
      DOI: 10.3390/jdb4020013
      Issue No: Vol. 4, No. 2 (2016)
  • JDB, Vol. 4, Pages 14: Hox Genes in Cardiovascular Development and

    • First page: 14
      Abstract: Congenital heart defects (CHD) are the leading cause of death in the first year of life. Over the past 20 years, much effort has been focused on unraveling the genetic bases of CHD. In particular, studies in human genetics coupled with those of model organisms have provided valuable insights into the gene regulatory networks underlying CHD pathogenesis. Hox genes encode transcription factors that are required for the patterning of the anterior–posterior axis in the embryo. In this review, we focus on the emerging role of anteriorly expressed Hox genes (Hoxa1, Hoxb1, and Hoxa3) in cardiac development, specifically their contribution to patterning of cardiac progenitor cells and formation of the great arteries. Recent evidence regarding the cooperative regulation of heart development by Hox proteins with members of the TALE-class of homeodomain proteins such as Pbx and Meis transcription factors is also discussed. These findings are highly relevant to human pathologies as they pinpoint new genes that increase susceptibility to cardiac anomalies and provide novel mechanistic insights into CHD.
      PubDate: 2016-03-24
      DOI: 10.3390/jdb4020014
      Issue No: Vol. 4, No. 2 (2016)
  • JDB, Vol. 4, Pages 15: Functional and Comparative Genomics of Hoxa2 Gene
           cis-Regulatory Elements: Evidence for Evolutionary Modification of
           Ancestral Core Element Activity

    • Authors: Adam Davis, Michael Reubens, Edmund Stellwag
      First page: 15
      Abstract: Hoxa2 is an evolutionarily conserved developmental regulatory gene that functions to specify rhombomere (r) and pharyngeal arch (PA) identities throughout the Osteichthyes. Japanese medaka (Oryzias latipes) hoxa2a, like orthologous Hoxa2 genes from other osteichthyans, is expressed during embryogenesis in r2–7 and PA2-7, whereas the paralogous medaka pseudogene, ψhoxa2b, is expressed in noncanonical Hoxa2 domains, including the pectoral fin buds. To understand the evolution of cis-regulatory element (CRE) control of gene expression, we conducted eGFP reporter gene expression studies with extensive functional mapping of several conserved CREs upstream of medaka hoxa2a and ψhoxa2b in transient and stable-line transgenic medaka embryos. The CREs tested were previously shown to contribute to directing mouse Hoxa2 gene expression in r3, r5, and PA2-4. Our results reveal the presence of sequence elements embedded in the medaka hoxa2a and ψhoxa2b upstream enhancer regions (UERs) that mediate expression in r4 and the PAs (hoxa2a r4/CNCC element) or in r3–7 and the PAs ψhoxa2b r3–7/CNCC element), respectively. Further, these elements were shown to be highly conserved among osteichthyans, which suggests that the r4 specifying element embedded in the UER of Hoxa2 is a deeply rooted rhombomere specifying element and the activity of this element has been modified by the evolution of flanking sequences that redirect its activity to alternative developmental compartments.
      PubDate: 2016-03-26
      DOI: 10.3390/jdb4020015
      Issue No: Vol. 4, No. 2 (2016)
  • JDB, Vol. 4, Pages 16: Mechanisms of Specificity for Hox Factor Activity

    • Authors: Arya Zandvakili, Brian Gebelein
      First page: 16
      Abstract: Metazoans encode clusters of paralogous Hox genes that are critical for proper development of the body plan. However, there are a number of unresolved issues regarding how paralogous Hox factors achieve specificity to control distinct cell fates. First, how do Hox paralogs, which have very similar DNA binding preferences in vitro, drive different transcriptional programs in vivo' Second, the number of potential Hox binding sites within the genome is vast compared to the number of sites bound. Hence, what determines where in the genome Hox factors bind' Third, what determines whether a Hox factor will activate or repress a specific target gene' Here, we review the current evidence that is beginning to shed light onto these questions. In particular, we highlight how cooperative interactions with other transcription factors (especially PBC and HMP proteins) and the sequences of cis-regulatory modules provide a basis for the mechanisms of Hox specificity. We conclude by integrating a number of the concepts described throughout the review in a case study of a highly interrogated Drosophila cis-regulatory module named “The Distal-less Conserved Regulatory Element” (DCRE).
      PubDate: 2016-05-09
      DOI: 10.3390/jdb4020016
      Issue No: Vol. 4, No. 2 (2016)
  • JDB, Vol. 4, Pages 17: Nutrient-Deprived Retinal Progenitors Proliferate
           in Response to Hypoxia: Interaction of the HIF-1 and mTOR Pathway

    • Authors: Helena Khaliullina, Nicola Love, William Harris
      First page: 17
      Abstract: At a cellular level, nutrients are sensed by the mechanistic Target of Rapamycin (mTOR). The response of cells to hypoxia is regulated via action of the oxygen sensor Hypoxia-Inducible Factor 1 (HIF-1). During development, injury and disease, tissues might face conditions of both low nutrient supply and low oxygen, yet it is not clear how cells adapt to both nutrient restriction and hypoxia, or how mTOR and HIF-1 interact in such conditions. Here we explore this question in vivo with respect to cell proliferation using the ciliary marginal zone (CMZ) of Xenopus. We found that both nutrient-deprivation and hypoxia cause retinal progenitors to decrease their proliferation, yet when nutrient-deprived progenitors are exposed to hypoxia there is an unexpected rise in cell proliferation. This increase, mediated by HIF-1 signalling, is dependent on glutaminolysis and reactivation of the mTOR pathway. We discuss how these findings in non-transformed tissue may also shed light on the ability of cancer cells in poorly vascularised solid tumours to proliferate.
      PubDate: 2016-05-19
      DOI: 10.3390/jdb4020017
      Issue No: Vol. 4, No. 2 (2016)
  • JDB, Vol. 4, Pages 18: Developmental Mechanism of Limb Field Specification
           along the Anterior–Posterior Axis during Vertebrate Evolution

    • Authors: Mikiko Tanaka
      First page: 18
      Abstract: In gnathostomes, limb buds arise from the lateral plate mesoderm at discrete positions along the body axis. Specification of these limb-forming fields can be subdivided into several steps. The lateral plate mesoderm is regionalized into the anterior lateral plate mesoderm (ALPM; cardiac mesoderm) and the posterior lateral plate mesoderm (PLPM). Subsequently, Hox genes appear in a nested fashion in the PLPM and provide positional information along the body axis. The lateral plate mesoderm then splits into the somatic and splanchnic layers. In the somatic layer of the PLPM, the expression of limb initiation genes appears in the limb-forming region, leading to limb bud initiation. Furthermore, past and current work in limbless amphioxus and lampreys suggests that evolutionary changes in developmental programs occurred during the acquisition of paired fins during vertebrate evolution. This review presents these recent advances and discusses the mechanisms of limb field specification during development and evolution, with a focus on the role of Hox genes in this process.
      PubDate: 2016-05-19
      DOI: 10.3390/jdb4020018
      Issue No: Vol. 4, No. 2 (2016)
  • JDB, Vol. 4, Pages 2: Hermes (Rbpms) is a Critical Component of RNP
           Complexes that Sequester Germline RNAs during Oogenesis

    • Authors: Tristan Aguero, Yi Zhou, Malgorzata Kloc, Patrick Chang, Evelyn Houliston, Mary King
      First page: 2
      Abstract: The germ cell lineage in Xenopus is specified by the inheritance of germ plasm that assembles within the mitochondrial cloud or Balbiani body in stage I oocytes. Specific RNAs, such as nanos1, localize to the germ plasm. nanos1 has the essential germline function of blocking somatic gene expression and thus preventing Primordial Germ Cell (PGC) loss and sterility. Hermes/Rbpms protein and nanos RNA co-localize within germinal granules, diagnostic electron dense particles found within the germ plasm. Previous work indicates that nanos accumulates within the germ plasm through a diffusion/entrapment mechanism. Here we show that Hermes/Rbpms interacts with nanos through sequence specific RNA localization signals found in the nanos-3′UTR. Importantly, Hermes/Rbpms specifically binds nanos, but not Vg1 RNA in the nucleus of stage I oocytes. In vitro binding data show that Hermes/Rbpms requires additional factors that are present in stage I oocytes in order to bind nanos1. One such factor may be hnRNP I, identified in a yeast-2-hybrid screen as directly interacting with Hermes/Rbpms. We suggest that Hermes/Rbpms functions as part of a RNP complex in the nucleus that facilitates selection of germline RNAs for germ plasm localization. We propose that Hermes/Rbpms is required for nanos RNA to form within the germinal granules and in this way, participates in the germline specific translational repression and sequestration of nanos RNA.
      PubDate: 2016-01-19
      DOI: 10.3390/jdb4010002
      Issue No: Vol. 4, No. 1 (2016)
  • JDB, Vol. 4, Pages 3: Notochord Cells in Intervertebral Disc Development
           and Degeneration

    • First page: 3
      Abstract: The intervertebral disc is a complex structure responsible for flexibility, multi-axial motion, and load transmission throughout the spine. Importantly, degeneration of the intervertebral disc is thought to be an initiating factor for back pain. Due to a lack of understanding of the pathways that govern disc degeneration, there are currently no disease-modifying treatments to delay or prevent degenerative disc disease. This review presents an overview of our current understanding of the developmental processes that regulate intervertebral disc formation, with particular emphasis on the role of the notochord and notochord-derived cells in disc homeostasis and how their loss can result in degeneration. We then describe the role of small animal models in understanding the development of the disc and their use to interrogate disc degeneration and associated pathologies. Finally, we highlight essential development pathways that are associated with disc degeneration and/or implicated in the reparative response of the tissue that might serve as targets for future therapeutic approaches.
      PubDate: 2016-01-21
      DOI: 10.3390/jdb4010003
      Issue No: Vol. 4, No. 1 (2016)
  • JDB, Vol. 4, Pages 4: Cell Fate Decisions During Breast Cancer Development

    • Authors: Kayla Gross, Ania Wronski, Adam Skibinski, Sarah Phillips, Charlotte Kuperwasser
      First page: 4
      Abstract: During the formation of breast cancer, many genes become altered as cells evolve progressively from normal to a pre-malignant to a malignant state of growth. How mutations in genes lead to specific subtypes of human breast cancer is only partially understood. Here we review how initial genetic or epigenetic alterations within mammary epithelial cells (MECs) can alter cell fate decisions and put pre-malignant cells on a path towards cancer development with specific phenotypes. Understanding the early stages of breast cancer initiation and progression and how normal developmental processes are hijacked during transformation has significant implications for improving early detection and prevention of breast cancer. In addition, insights gleaned from this understanding may also be important for developing subtype-specific treatment options.
      PubDate: 2016-01-22
      DOI: 10.3390/jdb4010004
      Issue No: Vol. 4, No. 1 (2016)
  • JDB, Vol. 4, Pages 5: Acknowledgement to Reviewers of Journal of
           Developmental Biology in 2015

    • Authors: Journal of Developmental Biology Editorial Office
      First page: 5
      Abstract: The editors of Journal of Developmental Biology would like to express their sincere gratitude to the following reviewers for assessing manuscripts in 2015. [...]
      PubDate: 2016-01-25
      DOI: 10.3390/jdb4010005
      Issue No: Vol. 4, No. 1 (2016)
  • JDB, Vol. 4, Pages 6: Alterations in Synthesis and Repair of DNA during
           the Development of Loach Misgurnus fossilis

    • Authors: Leonid Gening, Andrei Lakhin, Irina Makarova, Valentina Nenasheva, Ludmila Andreeva, Vyacheslav Tarantul
      First page: 6
      Abstract: Using a modified radiolabeled primer extension method (we named this modification misGvA—“misincorporation of G versus A”) we have investigated the DNA synthesis and repair at early and late stages of development of loach Misgurnus fossilis. The misincorporation activity of DNA polymerase iota (Pol ι) in wild-type loach could not be detected by this method at any stage of loach development. In transgenic loach overexpressing human Pol ι we have shown that the bypassing of DNA synthesis arrest after incorporation of mismatched nucleotide by Pol ι (the T-stop) was not associated with this enzyme. Non-transgenic loach larvae are virtually lacking the capacity for error correction of DNA duplex containing a mismatched nucleotide. Such repair activity develops only in the adult fish. It appears that the initial stages of development are characterized by more intensive DNA synthesis, while in terminal stages the repair activities become more prominent. The misGvA approach clearly indicates substantial changes in the DNA synthesis intensity, although the role of particular replicative and repair DNA polymerases in this process requires further study.
      PubDate: 2016-01-27
      DOI: 10.3390/jdb4010006
      Issue No: Vol. 4, No. 1 (2016)
  • JDB, Vol. 4, Pages 7: Restricted Pax3 Deletion within the Neural Tube
           Results in Congenital Hydrocephalus

    • Authors: Hong-Ming Zhou, Simon Conway
      First page: 7
      Abstract: Congenital hydrocephalus is a common birth-defect whose developmental origins are poorly understood. Pax3-null mutants show defects in myogenesis, neural tube closure, neural crest morphogenesis, and heart development that, consequently, results in embryonic lethality. Here we demonstrate that conditional deletion of the mouse Pax3 transcription factor results in fully-penetrant congenital obstructive hydrocephalus. To identify the role of Pax3 during cranial development, we deleted Pax3 within the neuroepithelium (via Pax7−Cre), in the neural crest (via P0-Cre), and in both the neuroepithelium and the neural crest (via Wnt1-Cre). Only conditional mutants generated using Pax7−Cre or Wnt1-Cre developed early onset congenital hydrocephalus due to stenosis of the third ventricle, suggesting that loss of neuroepithelial Pax3 is sufficient to disturb third ventricle morphogenesis. Dilation of lateral ventricles occurs as early as E14.5, and lineage-mapping revealed that the neuroepithelial cells in the conditional mutants are present, but fail to undergo normal differentiation at the stenotic site. Concomitant with a narrowing of the mutant third ventricle, we detected ectopic apoptosis, reduced proliferation, and abnormal β-catenin localization. Furthermore, consistent with the overlapping expression pattern of Pax3 and Pax7 in early cranial neuroepithelium, we demonstrated a combinatorial role, as compound Pax3/Pax7 heterozygotes display partially-penetrant congenital hydrocephalus. These murine data provide an experimental paradigm underpinning clinical observations of the presence of PAX3 mutations in some hydrocephalic patients.
      PubDate: 2016-02-01
      DOI: 10.3390/jdb4010007
      Issue No: Vol. 4, No. 1 (2016)
  • JDB, Vol. 4, Pages 8: Solving Classification Problems for Large Sets of
           Protein Sequences with the Example of Hox and ParaHox Proteins

    • Authors: Stefanie Hueber, Tancred Frickey
      First page: 8
      Abstract: Phylogenetic methods are key to providing models for how a given protein family evolved. However, these methods run into difficulties when sequence divergence is either too low or too high. Here, we provide a case study of Hox and ParaHox proteins so that additional insights can be gained using a new computational approach to help solve old classification problems. For two (Gsx and Cdx) out of three ParaHox proteins the assignments differ between the currently most established view and four alternative scenarios. We use a non-phylogenetic, pairwise-sequence-similarity-based method to assess which of the previous predictions, if any, are best supported by the sequence-similarity relationships between Hox and ParaHox proteins. The overall sequence-similarities show Gsx to be most similar to Hox2–3, and Cdx to be most similar to Hox4–8. The results indicate that a purely pairwise-sequence-similarity-based approach can provide additional information not only when phylogenetic inference methods have insufficient information to provide reliable classifications (as was shown previously for central Hox proteins), but also when the sequence variation is so high that the resulting phylogenetic reconstructions are likely plagued by long-branch-attraction artifacts.
      PubDate: 2016-02-04
      DOI: 10.3390/jdb4010008
      Issue No: Vol. 4, No. 1 (2016)
  • JDB, Vol. 4, Pages 9: The Roles of Aquaporins in Plant Stress Responses

    • Authors: Zunaira Afzal, T. Howton, Yali Sun, M. Mukhtar
      First page: 9
      Abstract: Aquaporins are membrane channel proteins ubiquitously present in all kingdoms of life. Although aquaporins were originally discovered as water channels, their roles in the transport of small neutral solutes, gasses, and metal ions are now well established. Plants contain the largest number and greatest diversity of aquaporin homologs with diverse subcellular localization patterns, gating properties, and solute specificity. The roles of aquaporins in physiological functions throughout plant growth and development are well known. As an integral regulator of plant–water relations, they are presumed to play an important role in plant defense responses against biotic and abiotic stressors. This review highlights involvement of various aquaporin homologs in plant stress responses against a variety of environmental stresses that disturb plant cell osmotic balance and nutrient homeostasis.
      PubDate: 2016-02-04
      DOI: 10.3390/jdb4010009
      Issue No: Vol. 4, No. 1 (2016)
  • JDB, Vol. 4, Pages 10: HoxA Genes and the Fin-to-Limb Transition in

    • First page: 10
      Abstract: HoxA genes encode for important DNA-binding transcription factors that act during limb development, regulating primarily gene expression and, consequently, morphogenesis and skeletal differentiation. Within these genes, HoxA11 and HoxA13 were proposed to have played an essential role in the enigmatic evolutionary transition from fish fins to tetrapod limbs. Indeed, comparative gene expression analyses led to the suggestion that changes in their regulation might have been essential for the diversification of vertebrates’ appendages. In this review, we highlight three potential modifications in the regulation and function of these genes that may have boosted appendage evolution: (1) the expansion of polyalanine repeats in the HoxA11 and HoxA13 proteins; (2) the origin of +a novel long-non-coding RNA with a possible inhibitory function on HoxA11; and (3) the acquisition of cis-regulatory elements modulating 5’ HoxA transcription. We discuss the relevance of these mechanisms for appendage diversification reviewing the current state of the art and performing additional comparative analyses to characterize, in a phylogenetic framework, HoxA11 and HoxA13 expression, alanine composition within the encoded proteins, long-non-coding RNAs and cis-regulatory elements.
      PubDate: 2016-02-17
      DOI: 10.3390/jdb4010010
      Issue No: Vol. 4, No. 1 (2016)
  • JDB, Vol. 4, Pages 11: Histologic Assessment of Drug-Eluting Grafts
           Related to Implantation Site

    • First page: 11
      Abstract: Drug-eluting vascular prostheses represent a new direction in vascular surgery to reduce early thrombosis and late intimal hyperplasia for small calibre grafts. Subcutaneous implantation in rats is a rapid and cost-effective screening model to assess the drug-elution effect and could, to some extent, be useful to forecast results for vascular prostheses. We compared biological and histological responses to scaffolds in different implantation sites. Polycaprolactone (PCL), paclitaxel-loaded PCL (PCL-PTX) and dexamethasone-loaded PCL (PCL-DXM) electrospun scaffolds were implanted subcutaneously and in an infrarenal abdominal aortic model in rats for up to 12 weeks. At the conclusion of the study, a histological analysis was performed. Cellular graft invasion revealed differences in the progression of cellular infiltration between PCL-PTX and PCL/PCL-DXM groups in both models. Cell infiltration increased over time in the aortic model compared to the subcutaneous model for all groups. Cell counting revealed major differences in fibroblast, macrophage and giant cell graft colonisation in all groups and models over time. Macrophages and giant cells increased in the PCL aortic model; whereas in the subcutaneous model these cell types increased only after three weeks or even decreased in the drug-eluting PCL groups. Other major findings were observed only in the aortic replacement such as extracellular matrix deposition and neo-angiogenesis. The subcutaneous implant model can be used for screening, especially when drug-eluting effects are studied. However, major histological differences were observed in cell type reaction and depth of cell penetration compared to the aortic model. Our results demonstrate that the implantation site is a critical determinant of the biological response.
      PubDate: 2016-02-20
      DOI: 10.3390/jdb4010011
      Issue No: Vol. 4, No. 1 (2016)
  • JDB, Vol. 4, Pages 12: An Overview of Hox Genes in Lophotrochozoa:
           Evolution and Functionality

    • Authors: Marco Barucca, Adriana Canapa, Maria Biscotti
      First page: 12
      Abstract: Hox genes are regulators of animal embryonic development. Changes in the number and sequence of Hox genes as well as in their expression patterns have been related to the evolution of the body plan. Lophotrochozoa is a clade of Protostomia characterized by several phyla which show a wide morphological diversity. Despite that the works summarized in this review emphasize the fragmentary nature of the data available regarding the presence and expression of Hox genes, they also offer interesting insight into the evolution of the Hox cluster and the role played by Hox genes in several phyla. However, the number of genes involved in the cluster of the lophotrochozoan ancestor is still a question of debate. The data presented here suggest that at least nine genes were present while two other genes, Lox4 and Post-2, may either have been present in the ancestor or may have arisen as a result of duplication in the Brachiopoda-Mollusca-Annelida lineage. Spatial and temporal collinearity is a feature of Hox gene expression which was probably present in the ancestor of deuterostomes and protostomes. However, in Lophotrochozoa, it has been detected in only a few species belonging to Annelida and Mollusca.
      PubDate: 2016-03-19
      DOI: 10.3390/jdb4010012
      Issue No: Vol. 4, No. 1 (2016)
  • JDB, Vol. 4, Pages 1: Beyond the Mammalian Heart: Fish and Amphibians as a
           Model for Cardiac Repair and Regeneration

    • Authors: Kyle Jewhurst, Kelly McLaughlin
      First page: 1
      Abstract: The epidemic of heart disease, the leading cause of death worldwide, is made worse by the fact that the adult mammalian heart is especially poor at repair. Damage to the mammal heart—such as that caused by myocardial infarction—leads to scarring, resulting in cardiac dysfunction and heart failure. In contrast, the hearts of fish and urodele amphibians are capable of complete regeneration of cardiac tissue from multiple types of damage, with full restoration of functionality. In the last decades, research has revealed a wealth of information on how these animals are able to perform this remarkable feat, and non-mammalian models of heart repair have become a burgeoning new source of data on the morphological, cellular, and molecular processes necessary to heal cardiac damage. In this review we present the major findings from recent research on the underlying mechanisms of fish and amphibian heart regeneration. We also discuss the tools and techniques that have been developed to answer these important questions.
      PubDate: 2015-12-23
      DOI: 10.3390/jdb4010001
      Issue No: Vol. 4, No. 1 (2015)
  • JDB, Vol. 3, Pages 93-111: Pbx4 is Required for the Temporal Onset of
           Zebrafish Myocardial Differentiation

    • Authors: Robert Kao, Joel Rurik, Gist III, Xiu Dong, Mark Majesky, Lisa Maves
      Pages: 93 - 111
      Abstract: Proper control of the temporal onset of cellular differentiation is critical for regulating cell lineage decisions and morphogenesis during development. Pbx homeodomain transcription factors have emerged as important regulators of cellular differentiation. We previously showed, by using antisense morpholino knockdown, that Pbx factors are needed for the timely activation of myocardial differentiation in zebrafish. In order to gain further insight into the roles of Pbx factors in heart development, we show here that zebrafish pbx4 mutant embryos exhibit delayed onset of myocardial differentiation, such as delayed activation of tnnt2a expression in early cardiomyocytes in the anterior lateral plate mesoderm. We also observe delayed myocardial morphogenesis and dysmorphic patterning of the ventricle and atrium, consistent with our previous Pbx knock-down studies. In addition, we find that pbx4 mutant larvae have aberrant outflow tracts and defective expression of the proepicardial marker tbx18. Finally, we present evidence for Pbx expression in cardiomyocyte precursors as well as heterogeneous Pbx expression among the pan-cytokeratin-expressing proepicardial cells near the developing ventricle. In summary, our data show that Pbx4 is required for the proper temporal activation of myocardial differentiation and establish a basis for studying additional roles of Pbx factors in heart development.
      PubDate: 2015-11-12
      DOI: 10.3390/jdb3040093
      Issue No: Vol. 3, No. 4 (2015)
  • JDB, Vol. 3, Pages 112-128: Pigment Epithelium-Derived Factor (PEDF) is a
           Determinant of Stem Cell Fate: Lessons from an Ultra-Rare Disease

    • Authors: Usman Sagheer, Jingjing Gong, Chuhan Chung
      Pages: 112 - 128
      Abstract: PEDF is a secreted glycoprotein that is widely expressed by multiple organs. Numerous functional contributions have been attributed to PEDF with antiangiogenic, antitumor, anti-inflammatory, and neurotrophic properties among the most prominent. The discovery that null mutations in the PEDF gene results in Osteogenesis Imperfecta Type VI, a rare autosomal recessive bone disease characterized by multiple fractures, highlights a critical developmental function for this protein. This ultra-rare orphan disease has provided biological insights into previous studies that noted PEDF’s effects on various stem cell populations. In addition to bone development, PEDF modulates resident stem cell populations in the brain, muscle, and eye. Functional effects on human embryonic stem cells have also been demonstrated. An overview of recent advances in our understanding by which PEDF regulates stem cells and their potential clinical applications will be evaluated in this review.
      PubDate: 2015-11-20
      DOI: 10.3390/jdb3040112
      Issue No: Vol. 3, No. 4 (2015)
  • JDB, Vol. 3, Pages 129-157: Cell Fate Decision Making through Oriented
           Cell Division

    • Authors: Evan Dewey, Danielle Taylor, Christopher Johnston
      Pages: 129 - 157
      Abstract: The ability to dictate cell fate decisions is critical during animal development. Moreover, faithful execution of this process ensures proper tissue homeostasis throughout adulthood, whereas defects in the molecular machinery involved may contribute to disease. Evolutionarily conserved protein complexes control cell fate decisions across diverse tissues. Maintaining proper daughter cell inheritance patterns of these determinants during mitosis is therefore a fundamental step of the cell fate decision-making process. In this review, we will discuss two key aspects of this fate determinant segregation activity, cortical cell polarity and mitotic spindle orientation, and how they operate together to produce oriented cell divisions that ultimately influence daughter cell fate. Our focus will be directed at the principal underlying molecular mechanisms and the specific cell fate decisions they have been shown to control.
      PubDate: 2015-12-14
      DOI: 10.3390/jdb3040129
      Issue No: Vol. 3, No. 4 (2015)
  • JDB, Vol. 3, Pages 158-176: Col11a1 Regulates Bone Microarchitecture
           during Embryonic Development

    • Authors: Anthony Hafez, Ryan Squires, Amber Pedracini, Alark Joshi, Robert Seegmiller, Julia Oxford
      Pages: 158 - 176
      Abstract: Collagen XI alpha 1 (Col11a1) is an extracellular matrix molecule required for embryonic development with a role in both nucleating the formation of fibrils and regulating the diameter of heterotypic fibrils during collagen fibrillar assembly. Although found in many different tissues throughout the vertebrate body, Col11a1 plays an essential role in endochondral ossification. To further understand the function of Col11a1 in the process of bone formation, we compared skeletal mineralization in wild-type (WT) mice and Col11a1-deficient mice using X-ray microtomography (micro-CT) and histology. Changes in trabecular bone microstructure were observed and are presented here. Additionally, changes to the periosteal bone collar of developing long bones were observed and resulted in an increase in thickness in the case of Col11a1-deficient mice compared to WT littermates. Vertebral bodies were incompletely formed in the absence of Col11a1. The data demonstrate that Col11a1 depletion results in alteration to newly-formed bone and is consistent with a role for Col11a1 in mineralization. These findings indicate that expression of Col11a1 in the growth plate and perichondrium is essential for trabecular bone and bone collar formation during endochondral ossification. The observed changes to mineralized tissues further define the function of Col11a1.
      PubDate: 2015-12-16
      DOI: 10.3390/jdb3040158
      Issue No: Vol. 3, No. 4 (2015)
  • JDB, Vol. 3, Pages 177-192: Role of Chondrocytes in Cartilage Formation,
           Progression of Osteoarthritis and Cartilage Regeneration

    • Authors: Hemanth Akkiraju, Anja Nohe
      Pages: 177 - 192
      Abstract: Articular cartilage (AC) covers the diarthrodial joints and is responsible for the mechanical distribution of loads across the joints. The majority of its structure and function is controlled by chondrocytes that regulate Extracellular Matrix (ECM) turnover and maintain tissue homeostasis. Imbalance in their function leads to degenerative diseases like Osteoarthritis (OA). OA is characterized by cartilage degradation, osteophyte formation and stiffening of joints. Cartilage degeneration is a consequence of chondrocyte hypertrophy along with the expression of proteolytic enzymes. Matrix Metalloproteinases (MMPs) and A Disintegrin and Metalloproteinase with Thrombospondin Motifs (ADAMTS) are an example of these enzymes that degrade the ECM. Signaling cascades involved in limb patterning and cartilage repair play a role in OA progression. However, the regulation of these remains to be elucidated. Further the role of stem cells and mature chondrocytes in OA progression is unclear. The progress in cell based therapies that utilize Mesenchymal Stem Cell (MSC) infusion for cartilage repair may lead to new therapeutics in the long term. However, many questions are unanswered such as the efficacy of MSCs usage in therapy. This review focuses on the role of chondrocytes in cartilage formation and the progression of OA. Moreover, it summarizes possible alternative therapeutic approaches using MSC infusion for cartilage restoration.
      PubDate: 2015-12-18
      DOI: 10.3390/jdb3040177
      Issue No: Vol. 3, No. 4 (2015)
  • JDB, Vol. 3, Pages 90-92: On the Origin of Cells

    • Authors: Robert W. Dettman
      Pages: 90 - 92
      Abstract: While non-blood cell lineage has been studied for decades by developmental biologists, only recently has it been considered in disease. This is partly due to a lack of suitable reagents in experimental models, but it is also the result of a failure to understand the ability of cells to move or differentiate in pathological environments. This Editorial gives a quick overview of the Special Issue “Cell Fate Decisions in Development and Disease” and underscores the importance of understanding the mechanisms of cell fate determination and lineage.
      PubDate: 2015-09-23
      DOI: 10.3390/jdb3030090
      Issue No: Vol. 3, No. 3 (2015)
  • JDB, Vol. 3, Pages 25-56: Retinoic Acid and the Development of the

    • Authors: Gregory Kelly, Thomas Drysdale
      Pages: 25 - 56
      Abstract: Retinoic acid (RA) is an important signaling molecule in the development of the endoderm and an important molecule in protocols used to generate endodermal cell types from stem cells. In this review, we describe the RA signaling pathway and its role in the patterning and specification of the extra embryonic endoderm and different endodermal organs. The formation of endoderm is an ancient evolutionary feature and RA signaling appears to have coevolved with the vertebrate lineage. Towards that end, we describe how RA participates in many regulatory networks required for the formation of extraembryonic structures as well as the organs of the embryo proper.
      PubDate: 2015-04-20
      DOI: 10.3390/jdb3020025
      Issue No: Vol. 3, No. 2 (2015)
  • JDB, Vol. 3, Pages 57-70: Roles of Antioxidative Enzymes in Wound Healing

    • Authors: Toshihiro Kurahashi, Junichi Fujii
      Pages: 57 - 70
      Abstract: Since skin is the first barrier separating the body from the external environment, impaired wound healing can be life threatening to living organisms. Delayed healing processes are observed in animals under certain circumstances, such as advanced age, diabetes, and immunosuppression, but the underlying mechanisms of the abnormality remain elusive. Redox homeostasis is defined as the balance between the levels of reactive oxygen species (ROS) and antioxidants in which antioxidative enzymes play central roles in scavenging ROS. In addition to deleterious effects, ROS also exert beneficial functions on some cellular processes such as transducing phosphorylation signaling, but excessive antioxidants may impede the healing process. Hence, strict control over the amounts of antioxidants is desirable when applied for therapeutic purposes. Here we overview recent findings regarding the relationships between antioxidative enzymes and wound healing. Unveiling the role of antioxidative enzymes is expected to contribute to our understanding of the wound healing processes.
      PubDate: 2015-04-27
      DOI: 10.3390/jdb3020057
      Issue No: Vol. 3, No. 2 (2015)
  • JDB, Vol. 3, Pages 71-89: Regeneration of the Epiphysis Including the
           Articular Cartilage in the Injured Knees of the Lizard Podarcis muralis

    • Authors: Lorenzo Alibardi
      Pages: 71 - 89
      Abstract: Cartilage regeneration is massive during tail regeneration in lizards but little is known about cartilage regeneration in other body regions of the skeleton. The recovery capability of injured epiphyses of femur and tibia of lizard knees has been studied by histology and 5BrdU immunohistochemistry in lizards kept at high environmental temperatures. Lizard epiphyses contain a secondary ossified center of variable extension surrounded peripherally by an articular cartilage and basally by columns of chondrocytes that form the mataphyseal or growth plate. After injury of the knee epiphyses, a broad degeneration of the articular cartilage during the first days post-injury is present. However a rapid regeneration of cartilaginous tissue is observed from 7 to 14 days post-injury and by 21 days post-lesions, a large part of the epiphyses are reformed by new cartilage. Labeling with 5BrdU indicates that the proliferating cells are derived from both the surface of the articular cartilage and from the metaphyseal plate, two chondrogenic regions that appear proliferating also in normal, uninjured knees. Chondroblasts proliferate by interstitial multiplication forming isogenous groups with only a scant extracellular matrix that later increases. The high regenerative power of lizard articular cartilage appears related to the permanence of growing cartilaginous centers in the epiphyses of long bones such as those of the knee during adulthood. It is likely that these regions contain resident stem cells that give rise to new chondroblasts of the articular and metaphyseal cartilage during most of the lizard’s lifetime, but can produce an excess of cartilaginous tissues when stimulated by the lesion.
      PubDate: 2015-05-12
      DOI: 10.3390/jdb3020071
      Issue No: Vol. 3, No. 2 (2015)
  • JDB, Vol. 3, Pages 1: Acknowledgement to Reviewers of the Journal of
           Developmental Biology in 2014

    • Authors: JDB Office
      Pages: 1 - 1
      Abstract: The editors of the Journal of Developmental Biology would like to express their sincere gratitude to the following reviewers for assessing manuscripts in 2014:[...]
      PubDate: 2015-01-09
      DOI: 10.3390/jdb3010001
      Issue No: Vol. 3, No. 1 (2015)
  • JDB, Vol. 3, Pages 2-10: Strain-Dependent Gene Expression during Mouse
           Embryonic Palate Development

    • Authors: Jiu-Zhen Jin, Jixiang Ding
      Pages: 2 - 10
      Abstract: The effect of strain background on gene function in growth and development has been well documented. However, it has not been extensively reported whether the strain background affects the gene expression pattern. Here, we found that the expression of homeobox gene Meox-2 and FGF receptor 1 gene Fgfr1 during mouse palate development is strain-dependent. On the C57B6 inbred background, Meox-2 is expressed in the palatal outgrowth on Embryonic Day 11.5 (E11.5); the expression shifts posteriorly and is restricted to the back of palate on E14.5. On the Swiss Webster outbred background, Meox-2 expression covers both anterior and posterior regions with the same intensity from E12.5 to E14.5. On the Black Swiss background, Meox-2 expression also covers the entire palate A-P axis, but is much weaker in the anterior region on E14.5. Fgfr1 also displays distinct expression patterns in the palatal outgrowth on E11.5 in these three strains. On the Black Swiss outbred background, the expression is restricted to the anterior palatal outgrowth. In marked contrast, the expression in the Swiss Webster outbred strain is located exclusively in the posterior palate outgrowth on E11.5, whereas in the C57B6 inbred strain, the expression is undetectable in the palatal outgrowth on E11.5.
      PubDate: 2015-02-06
      DOI: 10.3390/jdb3010002
      Issue No: Vol. 3, No. 1 (2015)
  • JDB, Vol. 3, Pages 11-24: Inhibition of SERPINE1 Function Attenuates Wound
           Closure in Response to Tissue Injury: A Role for PAI-1 in
           Re-Epithelialization and Granulation Tissue Formation

    • Authors: Tessa Simone, Paul Higgins
      Pages: 11 - 24
      Abstract: Plasminogen activator inhibitor-1 (PAI-1; SERPINE1) is a prominent member of the serine protease inhibitor superfamily (SERPIN) and a causative factor of multi-organ fibrosis as well as a key regulator of the tissue repair program. PAI-1 attenuates pericellular proteolysis by inhibiting the catalytic activity of both urokinase and tissue-type protease activators (uPA and tPA) effectively modulating, thereby, plasmin-mediated fibrinolysis and the overall pericellular proteolytic cascade. PAI-1 also impacts cellular responses to tissue injury and stress situations (growth, survival, migration) by titering the locale and temporal activation of multimeric cell-surface signaling complexes. This review will describe PAI-1 structure and function and detail the role of PAI-1 in the tissue repair program with an emphasis on cutaneous wound healing.
      PubDate: 2015-03-02
      DOI: 10.3390/jdb3010011
      Issue No: Vol. 3, No. 1 (2015)
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