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Development of the Brain in Health and Disease
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Development of the Brain in Health and Disease

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

Deadline for manuscript submissions: closed (31 August 2017) | Viewed by 28799

Special Issue Editor

Prof. Dr. Nicholas D.E. Greene

E-Mail Website
Guest Editor
Developmental Biology & Cancer Programme, UCL Great Ormond Street Institute of Child Health, University College London, London, UK
Interests: neural tube closure; birth defects; folate metabolism; gene-environment interactions; mouse development

Special Issue Information

Dear Colleagues,

The development of the brain depends on specification of the neuroepithelium, regulated tissue movements to generate the closed neural tube and patterning of the dorso-ventral and anterior-posterior axes. Subsequent coordinated growth, timely differentiation of appropriate cell types at precise positions, and establishment of connectivity are essential for brain function. Abnormalities during these developmental processes can lead to structural birth defects, such as holoprosencephaly, neural tube defects, and microcephaly, as well as later functional deficits manifesting as neurological impairment, intellectual disability and epilepsy. The detailed mechanisms underlying these highly complex processes are still the subject of intense research of importance both in understanding the fundamental process in development and the mechanisms underlying disease. This Special Issue of the Journal of Developmental Biology is intended to provide an overview of current progress in this large research field. Contributions can include original research papers or reviews.

Prof. Dr. Nicholas D.E. Greene
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

  • neural differentiation
  • neuronal migration
  • brain development
  • birth defects
  • central nervous system
  • neural tube
  • neural crest

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Published Papers (3 papers)

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Research

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4079 KiB  
Article
Ttc21b Is Required in Bergmann Glia for Proper Granule Cell Radial Migration
by Ashley M. Driver, Christopher Shumrick and Rolf W. Stottmann
J. Dev. Biol. 2017, 5(4), 18; https://doi.org/10.3390/jdb5040018 - 19 Dec 2017
Cited by 10 | Viewed by 6008
Abstract
Proper cerebellar development is dependent on tightly regulated proliferation, migration, and differentiation events. Disruptions in any of these leads to a range of cerebellar phenotypes from ataxia to childhood tumors. Animal models have shown that proper regulation of sonic hedgehog (Shh) [...] Read more.
Proper cerebellar development is dependent on tightly regulated proliferation, migration, and differentiation events. Disruptions in any of these leads to a range of cerebellar phenotypes from ataxia to childhood tumors. Animal models have shown that proper regulation of sonic hedgehog (Shh) signaling is crucial for normal cerebellar architecture, and increased signaling leads to cerebellar tumor formation. Primary cilia are known to be required for the proper regulation of multiple developmental signaling pathways, including Shh. Tetratricopeptide Repeat Domain 21B (Ttc21b) is required for proper primary cilia form and function, and is primarily thought to restrict Shh signaling. Here we investigated a role for Ttc21b in cerebellar development. Surprisingly, Ttc21b ablation in Bergmann glia resulted in the accumulation of ectopic granule cells in the lower/posterior lobes of the cerebellum and a reduction in Shh signaling. Ttc21b ablation in just Purkinje cells resulted in a similar phenotype seen in fewer cells, but across the entire extent of the cerebellum. These results suggest that Ttc21b expression is required for Bergmann glia structure and signaling in the developing cerebellum, and in some contexts, augments rather than attenuates Shh signaling. Full article
(This article belongs to the Special Issue Development of the Brain in Health and Disease)
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Review

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40 pages, 1601 KiB  
Review
Insights into the Etiology of Mammalian Neural Tube Closure Defects from Developmental, Genetic and Evolutionary Studies
by Diana M. Juriloff and Muriel J. Harris
J. Dev. Biol. 2018, 6(3), 22; https://doi.org/10.3390/jdb6030022 - 21 Aug 2018
Cited by 44 | Viewed by 11435
Abstract
The human neural tube defects (NTD), anencephaly, spina bifida and craniorachischisis, originate from a failure of the embryonic neural tube to close. Human NTD are relatively common and both complex and heterogeneous in genetic origin, but the genetic variants and developmental mechanisms are [...] Read more.
The human neural tube defects (NTD), anencephaly, spina bifida and craniorachischisis, originate from a failure of the embryonic neural tube to close. Human NTD are relatively common and both complex and heterogeneous in genetic origin, but the genetic variants and developmental mechanisms are largely unknown. Here we review the numerous studies, mainly in mice, of normal neural tube closure, the mechanisms of failure caused by specific gene mutations, and the evolution of the vertebrate cranial neural tube and its genetic processes, seeking insights into the etiology of human NTD. We find evidence of many regions along the anterior–posterior axis each differing in some aspect of neural tube closure—morphology, cell behavior, specific genes required—and conclude that the etiology of NTD is likely to be partly specific to the anterior–posterior location of the defect and also genetically heterogeneous. We revisit the hypotheses explaining the excess of females among cranial NTD cases in mice and humans and new developments in understanding the role of the folate pathway in NTD. Finally, we demonstrate that evidence from mouse mutants strongly supports the search for digenic or oligogenic etiology in human NTD of all types. Full article
(This article belongs to the Special Issue Development of the Brain in Health and Disease)
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2858 KiB  
Review
The α-Tubulin gene TUBA1A in Brain Development: A Key Ingredient in the Neuronal Isotype Blend
by Jayne Aiken, Georgia Buscaglia, Emily A. Bates and Jeffrey K. Moore
J. Dev. Biol. 2017, 5(3), 8; https://doi.org/10.3390/jdb5030008 - 19 Sep 2017
Cited by 47 | Viewed by 10700
Abstract
Microtubules are dynamic cytoskeletal polymers that mediate numerous, essential functions such as axon and dendrite growth and neuron migration throughout brain development. In recent years, sequencing has revealed dominant mutations that disrupt the tubulin protein building blocks of microtubules. These tubulin mutations lead [...] Read more.
Microtubules are dynamic cytoskeletal polymers that mediate numerous, essential functions such as axon and dendrite growth and neuron migration throughout brain development. In recent years, sequencing has revealed dominant mutations that disrupt the tubulin protein building blocks of microtubules. These tubulin mutations lead to a spectrum of devastating brain malformations, complex neurological and physical phenotypes, and even fatality. The most common tubulin gene mutated is the α-tubulin gene TUBA1A, which is the most prevalent α-tubulin gene expressed in post-mitotic neurons. The normal role of TUBA1A during neuronal maturation, and how mutations alter its function to produce the phenotypes observed in patients, remains unclear. This review synthesizes current knowledge of TUBA1A function and expression during brain development, and the brain malformations caused by mutations in TUBA1A. Full article
(This article belongs to the Special Issue Development of the Brain in Health and Disease)
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