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J. Dev. Biol., Volume 7, Issue 3 (September 2019) – 5 articles

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13 pages, 9785 KiB  
Article
Blood Vessel Patterning on Retinal Astrocytes Requires Endothelial Flt-1 (VEGFR-1)
by John C. Chappell, Jordan Darden, Laura Beth Payne, Kathryn Fink and Victoria L. Bautch
J. Dev. Biol. 2019, 7(3), 18; https://0-doi-org.brum.beds.ac.uk/10.3390/jdb7030018 - 07 Sep 2019
Cited by 7 | Viewed by 3967
Abstract
Feedback mechanisms are critical components of many pro-angiogenic signaling pathways that keep vessel growth within a functional range. The Vascular Endothelial Growth Factor-A (VEGF-A) pathway utilizes the decoy VEGF-A receptor Flt-1 to provide negative feedback regulation of VEGF-A signaling. In this study, we [...] Read more.
Feedback mechanisms are critical components of many pro-angiogenic signaling pathways that keep vessel growth within a functional range. The Vascular Endothelial Growth Factor-A (VEGF-A) pathway utilizes the decoy VEGF-A receptor Flt-1 to provide negative feedback regulation of VEGF-A signaling. In this study, we investigated how the genetic loss of flt-1 differentially affects the branching complexity of vascular networks in tissues despite similar effects on endothelial sprouting. We selectively ablated flt-1 in the post-natal retina and found that maximum induction of flt-1 loss resulted in alterations in endothelial sprouting and filopodial extension, ultimately yielding hyper-branched networks in the absence of changes in retinal astrocyte architecture. The mosaic deletion of flt-1 revealed that sprouting endothelial cells flanked by flt-1/ regions of vasculature more extensively associated with underlying astrocytes and exhibited aberrant sprouting, independent of the tip cell genotype. Overall, our data support a model in which tissue patterning features, such as retinal astrocytes, integrate with flt-1-regulated angiogenic molecular and cellular mechanisms to yield optimal vessel patterning for a given tissue. Full article
(This article belongs to the Special Issue Women in Developmental Biology)
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13 pages, 2868 KiB  
Article
Integrins Have Cell-Type-Specific Roles in the Development of Motor Neuron Connectivity
by Devyn Oliver, Emily Norman, Heather Bates, Rachel Avard, Monika Rettler, Claire Y. Bénard, Michael M. Francis and Michele L. Lemons
J. Dev. Biol. 2019, 7(3), 17; https://0-doi-org.brum.beds.ac.uk/10.3390/jdb7030017 - 27 Aug 2019
Cited by 1 | Viewed by 5976
Abstract
Formation of the nervous system requires a complex series of events including proper extension and guidance of neuronal axons and dendrites. Here we investigate the requirement for integrins, a class of transmembrane cell adhesion receptors, in regulating these processes across classes of C. [...] Read more.
Formation of the nervous system requires a complex series of events including proper extension and guidance of neuronal axons and dendrites. Here we investigate the requirement for integrins, a class of transmembrane cell adhesion receptors, in regulating these processes across classes of C. elegans motor neurons. We show α integrin/ina-1 is expressed by both GABAergic and cholinergic motor neurons. Despite this, our analysis of hypomorphic ina-1(gm144) mutants indicates preferential involvement of α integrin/ina-1 in GABAergic commissural development, without obvious involvement in cholinergic commissural development. The defects in GABAergic commissures of ina-1(gm144) mutants included both premature termination and guidance errors and were reversed by expression of wild type ina-1 under control of the native ina-1 promoter. Our results also show that α integrin/ina-1 is important for proper outgrowth and guidance of commissures from both embryonic and post-embryonic born GABAergic motor neurons, indicating an ongoing requirement for integrin through two phases of GABAergic neuron development. Our findings provide insights into neuron-specific roles for integrin that would not be predicted based solely upon expression analysis. Full article
(This article belongs to the Special Issue Caenorhabditis elegans - A Developmental Genetic Model System)
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37 pages, 1744 KiB  
Review
The Molecular Basis of Human Anophthalmia and Microphthalmia
by Philippa Harding and Mariya Moosajee
J. Dev. Biol. 2019, 7(3), 16; https://0-doi-org.brum.beds.ac.uk/10.3390/jdb7030016 - 14 Aug 2019
Cited by 43 | Viewed by 12725
Abstract
Human eye development is coordinated through an extensive network of genetic signalling pathways. Disruption of key regulatory genes in the early stages of eye development can result in aborted eye formation, resulting in an absent eye (anophthalmia) or a small underdeveloped eye (microphthalmia) [...] Read more.
Human eye development is coordinated through an extensive network of genetic signalling pathways. Disruption of key regulatory genes in the early stages of eye development can result in aborted eye formation, resulting in an absent eye (anophthalmia) or a small underdeveloped eye (microphthalmia) phenotype. Anophthalmia and microphthalmia (AM) are part of the same clinical spectrum and have high genetic heterogeneity, with >90 identified associated genes. By understanding the roles of these genes in development, including their temporal expression, the phenotypic variation associated with AM can be better understood, improving diagnosis and management. This review describes the genetic and structural basis of eye development, focusing on the function of key genes known to be associated with AM. In addition, we highlight some promising avenues of research involving multiomic approaches and disease modelling with induced pluripotent stem cell (iPSC) technology, which will aid in developing novel therapies. Full article
(This article belongs to the Special Issue Women in Developmental Biology)
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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://0-doi-org.brum.beds.ac.uk/10.3390/jdb7030015 - 12 Jul 2019
Cited by 3 | Viewed by 4300
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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8 pages, 1924 KiB  
Review
The Role of Hedgehog Signaling in Adult Lung Regeneration and Maintenance
by Chaoqun Wang, Monica Cassandras and Tien Peng
J. Dev. Biol. 2019, 7(3), 14; https://0-doi-org.brum.beds.ac.uk/10.3390/jdb7030014 - 09 Jul 2019
Cited by 19 | Viewed by 4992
Abstract
As a secreted morphogen, Sonic Hedgehog (SHH) determines differential cell fates, behaviors, and functions by forming a gradient of Hedgehog (Hh) activation along an axis of Hh-receptive cells during development. Despite clearly delineated roles for Hh during organ morphogenesis, whether Hh continues to [...] Read more.
As a secreted morphogen, Sonic Hedgehog (SHH) determines differential cell fates, behaviors, and functions by forming a gradient of Hedgehog (Hh) activation along an axis of Hh-receptive cells during development. Despite clearly delineated roles for Hh during organ morphogenesis, whether Hh continues to regulate cell fate and behavior in the same fashion in adult organs is less understood. Adult organs, particularly barrier organs interfacing with the ambient environment, are exposed to insults that require renewal of cellular populations to maintain structural integrity. Understanding key aspects of Hh’s ability to generate an organ could translate into conceptual understanding of Hh’s ability to maintain organ homeostasis and stimulate regeneration. In this review, we will summarize the current knowledge about Hh signaling in regulating adult lung regeneration and maintenance, and discuss how alteration of Hh signaling contributes to adult lung diseases. Full article
(This article belongs to the Collection Hedgehog Signaling in Embryogenesis)
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