Talk:Developmental Mechanism - Apoptosis
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Cite this page: Hill, M.A. (2024, April 18) Embryology Developmental Mechanism - Apoptosis. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Developmental_Mechanism_-_Apoptosis |
10 Most Recent Papers
Note - This sub-heading shows an automated computer PubMed search using the listed sub-heading term. References appear in this list based upon the date of the actual page viewing. Therefore the list of references do not reflect any editorial selection of material based on content or relevance. In comparison, references listed on the content page and discussion page (under the publication year sub-headings) do include editorial selection based upon relevance and availability. (More? Pubmed Most Recent)
Developmental Apoptosis
<pubmed limit=10>Developmental Apoptosis</pubmed>
2018
Caspases and matrix metalloproteases facilitate collective behavior of non-neural ectoderm after hindbrain neuropore closure
BMC Dev Biol. 2018 Jul 31;18(1):17. doi: 10.1186/s12861-018-0175-3.
Shinotsuka N1, Yamaguchi Y2,3, Nakazato K4, Matsumoto Y1, Mochizuki A4,5, Miura M6.
Abstract BACKGROUND: Mammalian brain is formed through neural tube closure (NTC), wherein both ridges of opposing neural folds are fused in the midline and remodeled in the roof plate of the neural tube and overlying non-neural ectodermal layer. Apoptosis is widely observed from the beginning of NTC at the neural ridges and is crucial for the proper progression of NTC, but its role after the closure remains less clear. RESULTS: Here, we conducted live-imaging analysis of the mid-hindbrain neuropore (MHNP) closure and revealed unexpected collective behavior of cells surrounding the MHNP. The cells first gathered to the closing point and subsequently relocated as if they were released from the point. Inhibition of caspases or matrix metalloproteases with chemical inhibitors impaired the cell relocation. CONCLUSIONS: These lines of evidence suggest that apoptosis-mediated degradation of extracellular matrix might facilitate the final process of neuropore closure. KEYWORDS: Apoptosis; Caspases; Live-imaging; Matrix metalloproteases; Neural tube closure PMID: 30064364 DOI: 10.1186/s12861-018-0175-3
2017
p63 exerts spatio-temporal control of palatal epithelial cell fate to prevent cleft palate
PLoS Genet. 2017 Jun 12;13(6):e1006828. doi: 10.1371/journal.pgen.1006828. eCollection 2017 Jun.
Richardson R1, Mitchell K1, Hammond NL1, Mollo MR2, Kouwenhoven EN3, Wyatt ND1, Donaldson IJ1, Zeef L1, Burgis T1, Blance R1, van Heeringen SJ3, Stunnenberg HG4, Zhou H3,5, Missero C2,6, Romano RA7, Sinha S8, Dixon MJ1, Dixon J1. Author information Abstract Cleft palate is a common congenital disorder that affects up to 1 in 2500 live births and results in considerable morbidity to affected individuals and their families. The aetiology of cleft palate is complex with both genetic and environmental factors implicated. Mutations in the transcription factor p63 are one of the major individual causes of cleft palate; however, the gene regulatory networks in which p63 functions remain only partially characterized. Our findings demonstrate that p63 functions as an essential regulatory molecule in the spatio-temporal control of palatal epithelial cell fate to ensure appropriate fusion of the palatal shelves. Initially, p63 induces periderm formation and controls its subsequent maintenance to prevent premature adhesion between adhesion-competent, intra-oral epithelia. Subsequently, TGFβ3-induced down-regulation of p63 in the medial edge epithelia of the palatal shelves is a pre-requisite for palatal fusion by facilitating periderm migration from, and reducing the proliferative potential of, the midline epithelial seam thereby preventing cleft palate. PMID: 28604778 PMCID: PMC5484519 DOI: 10.1371/journal.pgen.1006828
p63 gene encodes multiple isotypes with remarkably divergent abilities to transactivate p53 reporter genes and induce apoptosis.
2011
Type I vs type II spiral ganglion neurons exhibit differential survival and neuritogenesis during cochlear development
Neural Dev. 2011 Oct 11;6:33.
Barclay M, Ryan AF, Housley GD. Source Department of Physiology, The University of Auckland, Private Bag 92019, Auckland, New Zealand. g.housley@unsw.edu.au. Abstract ABSTRACT:
BACKGROUND: The mechanisms that consolidate neural circuitry are a major focus of neuroscience. In the mammalian cochlea, the refinement of spiral ganglion neuron (SGN) innervation to the inner hair cells (by type I SGNs) and the outer hair cells (by type II SGNs) is accompanied by a 25% loss of SGNs.
RESULTS: We investigated the segregation of neuronal loss in the mouse cochlea using β-tubulin and peripherin antisera to immunolabel all SGNs and selectively type II SGNs, respectively, and discovered that it is the type II SGN population that is predominately lost within the first postnatal week. Developmental neuronal loss has been attributed to the decline in neurotrophin expression by the target hair cells during this period, so we next examined survival of SGN sub-populations using tissue culture of the mid apex-mid turn region of neonatal mouse cochleae. In organotypic culture for 48 hours from postnatal day 1, endogenous trophic support from the organ of Corti proved sufficient to maintain all type II SGNs; however, a large proportion of type I SGNs were lost. Culture of the spiral ganglion as an explant, with removal of the organ of Corti, led to loss of the majority of both SGN sub-types. Brain-derived neurotrophic factor (BDNF) added as a supplement to the media rescued a significant proportion of the SGNs, particularly the type II SGNs, which also showed increased neuritogenesis. The known decline in BDNF production by the rodent sensory epithelium after birth is therefore a likely mediator of type II neuron apoptosis.
CONCLUSION: Our study thus indicates that BDNF supply from the organ of Corti supports consolidation of type II innervation in the neonatal mouse cochlea. In contrast, type I SGNs likely rely on additional sources for trophic support.
PMID 21989106
Who lives and who dies: Role of apoptosis in quashing developmental errors
Commun Integr Biol. 2011 Jul;4(4):495-7. Epub 2011 Jul 1.
Koto A, Miura M. Source Department of Genetics; Graduate School of Pharmaceutical Sciences; The University of Tokyo. Abstract Apoptosis is essential for normal development. Large numbers of cells are eliminated by apoptosis in early neural development and during the formation of neural connections. However, our understanding of this life-or-death decision is incomplete, because it is difficult to identify dying cells by conventional strategies. Live imaging is powerful for studying apoptosis, because it can trace a death-fated cell throughout its lifetime. The Drosophila sensory organ development is a convenient system for studying neural-cell selection via lateral inhibition. We recently showed that about 20% of the differentiating neuronal cells die during sensory organ development, which results in the characteristic spatial patterning of the sensory organs. The eliminated differentiating neurons expressed neurogenic genes and high levels of activated Notch. Thus, live imaging allowed us to document the role of apoptosis in neural progenitor selection, and revealed that Notch activation is the mechanism determining which cells die during sensory organ development.
PMID 21966582
