Talk:Neural - Tectum Development
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Cite this page: Hill, M.A. (2024, April 20) Embryology Neural - Tectum Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Neural_-_Tectum_Development |
2012
Thymosin β4 induces folding of the developing optic tectum in the chicken (Gallus domestics)
J Comp Neurol. 2012 Jun 1;520(8):1650-62. doi: 10.1002/cne.23004.
Wirsching HG, Kretz O, Morosan-Puopolo G, Chernogorova P, Theiss C, Brand-Saberi B. Source Department of Molecular Embryology, University of Freiburg, D-79104 Freiburg, Germany.
Abstract
Thymosin β4 (Tβ4) is a highly conserved G-actin binding polypeptide with multiple intra- and extracellular functions. While stem-cell activation as well as promotion of cell survival and migration by Tβ4 have been investigated in various in vitro and in vivo studies, there are few data on the implications of Tβ4 in brain development. In the present study we analyzed Tβ4 expression in the developing optic tectum of the chicken (Gallus domesticus) and performed in ovo retroviral transduction and plasmid electroporation for overexpression and knockdown of Tβ4. We found marked Tβ4 expression in the tectal plate and in all neuronal layers of later developmental stages, but not in the ventricular zone where neural stem cells reside and divide. Knockdown of Tβ4 inhibited growth of Tβ4-depleted hemispheres, whereas overexpression of Tβ4 led to the production of neuroepithelial folds resembling gyri and sulci, which are not normally present in avian brains. The mechanism yielding enhanced growth of Tβ4 overexpressing hemispheres involved enhanced proliferation, thus indicating an impact of Tβ4 on the neural stem cell and/or progenitor cell population. In summary, we found that due to its effects on proliferation, Tβ4 expression has a large impact on neuroepithelial and macroscopic brain development. Copyright © 2011 Wiley Periodicals, Inc.
PMID 22120963
Genetic and physical interaction of Meis2, Pax3 and Pax7 during dorsal midbrain development
BMC Dev Biol. 2012 Mar 5;12:10.
Agoston Z, Li N, Haslinger A, Wizenmann A, Schulte D. Source Institute of Neurology (Edinger Institute), J, W, Goethe University Medical School, Heinrich Hoffmannstr, 7, 50628 Frankfurt, Germany.
Abstract
BACKGROUND: During early stages of brain development, secreted molecules, components of intracellular signaling pathways and transcriptional regulators act in positive and negative feed-back or feed-forward loops at the mid-hindbrain boundary. These genetic interactions are of central importance for the specification and subsequent development of the adjacent mid- and hindbrain. Much less, however, is known about the regulatory relationship and functional interaction of molecules that are expressed in the tectal anlage after tectal fate specification has taken place and tectal development has commenced. RESULTS: Here, we provide experimental evidence for reciprocal regulation and subsequent cooperation of the paired-type transcription factors Pax3, Pax7 and the TALE-homeodomain protein Meis2 in the tectal anlage. Using in ovo electroporation of the mesencephalic vesicle of chick embryos we show that (i) Pax3 and Pax7 mutually regulate each other's expression in the mesencephalic vesicle, (ii) Meis2 acts downstream of Pax3/7 and requires balanced expression levels of both proteins, and (iii) Meis2 physically interacts with Pax3 and Pax7. These results extend our previous observation that Meis2 cooperates with Otx2 in tectal development to include Pax3 and Pax7 as Meis2 interacting proteins in the tectal anlage. CONCLUSION: The results described here suggest a model in which interdependent regulatory loops involving Pax3 and Pax7 in the dorsal mesencephalic vesicle modulate Meis2 expression. Physical interaction with Meis2 may then confer tectal specificity to a wide range of otherwise broadly expressed transcriptional regulators, including Otx2, Pax3 and Pax7. PMID 22390724
http://www.biomedcentral.com/1471-213X/12/10
Balancing of ephrin/Eph forward and reverse signaling as the driving force of adaptive topographic mapping
Development. 2012 Jan;139(2):335-45. Epub 2011 Dec 7.
Gebhardt C, Bastmeyer M, Weth F. Source Zoological Institute, Department of Cell- and Neurobiology, Karlsruhe Institute of Technology (KIT), Karlsruhe, Germany.
Abstract
The retinotectal projection, which topographically maps retinal axons onto the tectum of the midbrain, is an ideal model system with which to investigate the molecular genetics of embryonic brain wiring. Corroborating Sperry's seminal hypothesis, ephrin/Eph counter-gradients on both retina and tectum were found to represent matching chemospecificity markers. Intriguingly, however, it has never been possible to reconstitute topographically appropriate fiber growth in vitro with these cues. Moreover, experimentally derived molecular mechanisms have failed to provide explanations as to why the mapping adapts to grossly diverse targets in some experiments, while displaying strict point-to-point specificity in others. In vitro, ephrin-A/EphA forward, as well as reverse, signaling mediate differential repulsion to retinal fibers, instead of providing topographic guidance. We argue that those responses are indicative of ephrin-A and EphA being members of a guidance system that requires two counteracting cues per axis. Experimentally, we demonstrate by introducing novel double-cue stripe assays that the simultaneous presence of both cues indeed suffices to elicit topographically appropriate guidance. The peculiar mechanism, which uses forward and reverse signaling through a single receptor/ligand combination, entails fiber/fiber interactions. We therefore propose to extend Sperry's model to include ephrin-A/EphA-based fiber/fiber chemospecificity, eventually out-competing fiber/target interactions. By computational simulation, we show that our model is consistent with stripe assay results. More importantly, however, it not only accounts for classical in vivo evidence of point-to-point and adaptive topographic mapping, but also for the map duplication found in retinal EphA knock-in mice. Nonetheless, it is based on a single constraint of topographic growth cone navigation: the balancing of ephrin-A/EphA forward and reverse signalling.
PMID 22159582
2011
Notch signalling stabilises boundary formation at the midbrain-hindbrain organiser
Development. 2011 Sep;138(17):3745-57. Epub 2011 Jul 27.
Tossell K, Kiecker C, Wizenmann A, Lang E, Irving C. Source Department of Cell and Developmental Biology, University College London, Gower Street, London WC1E 6BT, UK.
Abstract
The midbrain-hindbrain interface gives rise to a boundary of particular importance in CNS development as it forms a local signalling centre, the proper functioning of which is essential for the formation of tectum and cerebellum. Positioning of the mid-hindbrain boundary (MHB) within the neuroepithelium is dependent on the interface of Otx2 and Gbx2 expression domains, yet in the absence of either or both of these genes, organiser genes are still expressed, suggesting that other, as yet unknown mechanisms are also involved in MHB establishment. Here, we present evidence for a role for Notch signalling in stabilising cell lineage restriction and regulating organiser gene expression at the MHB. Experimental interference with Notch signalling in the chick embryo disrupts MHB formation, including downregulation of the organiser signal Fgf8. Ectopic activation of Notch signalling in cells of the anterior hindbrain results in an exclusion of those cells from rhombomeres 1 and 2, and in a simultaneous clustering along the anterior and posterior boundaries of this area, suggesting that Notch signalling influences cell sorting. These cells ectopically express the boundary marker Fgf3. In agreement with a role for Notch signalling in cell sorting, anterior hindbrain cells with activated Notch signalling segregate from normal cells in an aggregation assay. Finally, misexpression of the Notch modulator Lfng or the Notch ligand Ser1 across the MHB leads to a shift in boundary position and loss of restriction of Fgf8 to the MHB. We propose that differential Notch signalling stabilises the MHB through regulating cell sorting and specifying boundary cell fate. PMID 21795283 [PubMed - indexed for MEDLINE] PMCID: PMC3152928
