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Matrix Remodelling during Development
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Matrix Remodelling during Development

A special issue of Journal of Developmental Biology (ISSN 2221-3759).

Deadline for manuscript submissions: closed (30 September 2019) | Viewed by 16527

Special Issue Editor

Prof. Dr. Bryan D. Crawford

E-Mail Website
Guest Editor
partment of Biology, University of New Brunswick, Fredericton, NB E3B 5A3, Canada
Interests: cell–matrix interactions; extracellular matrix remodeling; morphogenesis; tissue architecture; matrix metalloproteinases; microscopy and image processing; zebrafish

Special Issue Information

Dear Colleagues,

The emergence of functional tissue architecture, and the dramatic changes in tissue structure that occur during embryonic morphogenesis, require dynamic remodelling of the extracellular matrix (ECM). Yet our understanding of how cellular activities bring about these changes, how these activities are regulated, and how these regulatory mechanisms have evolved remain frustratingly vague. This Special Issue will focus on new data and novel insights into the remodelling of the extracellular matrix occurring during embryonic development, with emphasis on the underlying molecular mechanisms. We especially encourage submission of studies elucidating activities and regulation of ECM remodelling effectors in vivo, and investigations based on a broad phylogenetic perspective. Both research and review papers are welcome. The objective of this Special Issue is to contribute significantly to a coherent model of how genetically programmed cellular activity cooperatively give rise to meso- and macroscopic tissue organization.

Prof. Dr. Bryan D. Crawford
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Developmental Biology is an international peer-reviewed open access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Extracellular matrix
  • Matrix remodeling
  • Morphogenesis
  • MMPs
  • ADAMS
  • TIMPs
  • Adhesion
  • Biomechanics
  • Cell migration and pathfinding
  • Sequestered signaling molecules

Published Papers (4 papers)

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Research

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16 pages, 2389 KiB  
Article
Matrix Metalloproteinase 13 Activity is Required for Normal and Hypoxia-Induced Precocious Hatching in Zebrafish Embryos
by Christopher D. Small, Megan el-Khoury, Ghislain Deslongchamps, Tillmann J. Benfey and Bryan D. Crawford
J. Dev. Biol. 2020, 8(1), 3; https://doi.org/10.3390/jdb8010003 - 31 Jan 2020
Cited by 11 | Viewed by 2970
Abstract
Hypoxia induces precocious hatching in zebrafish, but we do not have a clear understanding of the molecular mechanisms regulating the activation of the hatching enzyme or how these mechanisms trigger precocious hatching under unfavorable environmental conditions. Using immunohistochemistry, pharmacological inhibition of matrix metalloproteinase [...] Read more.
Hypoxia induces precocious hatching in zebrafish, but we do not have a clear understanding of the molecular mechanisms regulating the activation of the hatching enzyme or how these mechanisms trigger precocious hatching under unfavorable environmental conditions. Using immunohistochemistry, pharmacological inhibition of matrix metalloproteinase 13 (Mmp13), and in vivo zymography, we show that Mmp13a is present in the hatching gland just as embryos become hatching competent and that Mmp13a activity is required for both normal hatching and hypoxia-induced precocious hatching. We conclude that Mmp13a likely functions in activating the hatching enzyme zymogen and that Mmp13a activity is necessary but not sufficient for hatching in zebrafish. This study highlights the broad nature of MMP function in development and provides a non-mammalian example of extra-embryonic processes mediated by MMP activity. Full article
(This article belongs to the Special Issue Matrix Remodelling during Development)
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18 pages, 14695 KiB  
Article
Paralogues of Mmp11 and Timp4 Interact during the Development of the Myotendinous Junction in the Zebrafish Embryo
by Emma F. Matchett, Shuaijin Wang and Bryan D. Crawford
J. Dev. Biol. 2019, 7(4), 22; https://doi.org/10.3390/jdb7040022 - 03 Dec 2019
Cited by 10 | Viewed by 3818
Abstract
The extracellular matrix (ECM) of the myotendinous junction (MTJ) undergoes dramatic physical and biochemical remodeling during the first 48 h of development in zebrafish, transforming from a rectangular fibronectin-dominated somite boundary to a chevron-shaped laminin-dominated MTJ. Matrix metalloproteinase 11 (Mmp11, a.k.a. Stromelysin-3) is [...] Read more.
The extracellular matrix (ECM) of the myotendinous junction (MTJ) undergoes dramatic physical and biochemical remodeling during the first 48 h of development in zebrafish, transforming from a rectangular fibronectin-dominated somite boundary to a chevron-shaped laminin-dominated MTJ. Matrix metalloproteinase 11 (Mmp11, a.k.a. Stromelysin-3) is both necessary and sufficient for the removal of fibronectin at the MTJ, but whether this protease acts directly on fibronectin and how its activity is regulated remain unknown. Using immunofluorescence, we show that both paralogues of Mmp11 accumulate at the MTJ during this time period, but with Mmp11a present early and later replaced by Mmp11b. Moreover, Mmp11a also accumulates intracellularly, associated with the Z-discs of sarcomeres within skeletal muscle cells. Using the epitope-mediated MMP activation (EMMA) assay, we show that despite having a weaker paired basic amino acid motif in its propeptide than Mmp11b, Mmp11a is activated by furin, but may also be activated by other mechanisms intracellularly. One or both paralogues of tissue inhibitors of metalloproteinase-4 (Timp4) are also present at the MTJ throughout this process, and yeast two-hybrid assays reveal distinct and specific interactions between various domains of these proteins. We propose a model in which Mmp11a activity is modulated (but not inhibited) by Timp4 during early MTJ remodeling, followed by a phase in which Mmp11b activity is both inhibited and spatially constrained by Timp4 in order to maintain the structural integrity of the mature MTJ. Full article
(This article belongs to the Special Issue Matrix Remodelling during Development)
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Graphical abstract

16 pages, 2700 KiB  
Article
Pectoral Fin Anomalies in tbx5a Knockdown Zebrafish Embryos Related to the Cascade Effect of N-Cadherin and Extracellular Matrix Formation
by Jenn-Kan Lu, Tzu-Chun Tsai, Hsinyu Lee, Kai Hsia, Chih-Hsun Lin and Jen-Her Lu
J. Dev. Biol. 2019, 7(3), 15; https://doi.org/10.3390/jdb7030015 - 12 Jul 2019
Cited by 3 | Viewed by 4360
Abstract
Functional knockdown of zebrafish tbx5a causes hypoplasia or aplasia of pectoral fins. This study aimed to assess developmental pectoral fin anomalies in tbx5a morpholino knockdown zebrafish embryos. The expression of cartilage-related genes in the tbx5a morphant was analyzed by DNA microarray, immunostaining, and [...] Read more.
Functional knockdown of zebrafish tbx5a causes hypoplasia or aplasia of pectoral fins. This study aimed to assess developmental pectoral fin anomalies in tbx5a morpholino knockdown zebrafish embryos. The expression of cartilage-related genes in the tbx5a morphant was analyzed by DNA microarray, immunostaining, and thin-section histology to examine the detailed distribution of the extracellular matrix (ECM) during different pectoral fin developmental stages. Chondrogenic condensation (CC) in the tbx5a morpholino knockdown group was barely recognizable at 37 h postfertilization (hpf); the process from CC to endoskeleton formation was disrupted at 48 hpf, and the endoskeleton was only loosely formed at 72 hpf. Microarrays identified 18 downregulated genes in tbx5a-deficient embryos, including 2 fin morphogenesis-related (cx43, bbs7), 4 fin development-related (hoxc8a, hhip, axin1, msxb), and 12 cartilage development-related (mmp14a, sec23b, tfap2a, slc35b2, dlx5a, dlx1a, tfap2b, fmr1, runx3, cdh2, lect1, acvr2a, mmp14b) genes, at 24 and 30 hpf. The increase in apoptosis-related proteins (BAD and BCL2) in the tbx5a morphant influenced the cellular component of pectoral fins and resulted in chondrocyte reduction throughout the different CC phases. Furthermore, tbx5a knockdown interfered with ECM formation in pectoral fins, affecting glycosaminoglycans, fibronectin, hyaluronic acid (HA), and N-cadherin. Our results provide evidence that the pectoral fin phenotypic anomaly induced by tbx5a knockdown is related to disruption of the mesoderm and ECM, consequently interfering with mesoderm migration, CC, and subsequent endoskeleton formation. Full article
(This article belongs to the Special Issue Matrix Remodelling during Development)
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Review

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13 pages, 1293 KiB  
Review
A Potential Role for MMPs during the Formation of Non-Neurogenic Placodes
by Paige M. Drake and Tamara A. Franz-Odendaal
J. Dev. Biol. 2018, 6(3), 20; https://doi.org/10.3390/jdb6030020 - 26 Jul 2018
Cited by 2 | Viewed by 4471
Abstract
The formation of non-neurogenic placodes is critical prior to the development of several epithelial derivatives (e.g., feathers, teeth, etc.) and their development frequently involves morphogenetic proteins (or morphogens). Matrix metalloproteinases (MMPs) are important enzymes involved in extracellular matrix remodeling, and recent research has [...] Read more.
The formation of non-neurogenic placodes is critical prior to the development of several epithelial derivatives (e.g., feathers, teeth, etc.) and their development frequently involves morphogenetic proteins (or morphogens). Matrix metalloproteinases (MMPs) are important enzymes involved in extracellular matrix remodeling, and recent research has shown that the extracellular matrix (ECM) can modulate morphogen diffusion and cell behaviors. This review summarizes the known roles of MMPs during the development of non-neurogenic structures that involve a placodal stage. Specifically, we discuss feather, hair, tooth, mammary gland and lens development. This review highlights the potential critical role MMPs may play during placode formation in these systems. Full article
(This article belongs to the Special Issue Matrix Remodelling during Development)
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