Cell death in the gastrulating chick embryo: potential roles for tumor necrosis factor-alpha (TNF-α)

Sanders, Esmond J.; Prasad, S.; Hu, Ninghe; Wride, Michael A.

doi:10.1038/sj.cdd.4400235

Cited by 11 publications

(6 citation statements)

References 62 publications

(84 reference statements)

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“…As the neural plate arises, TUNEL-positive cells accumulate at the edge of the Dad1-expressing domain, forming an arc at the border of the neural plate (future neural crest and placode area) and proximal non-neural ectoderm. These regions retain a higher incidence of apoptosis at later stages of development (Graham et al, 1993, Hensey and Gautier, 1998, Sanders et al, 1997a, Sanders et al, 1997b, Wride et al, 1994. In our experiments, misexpression of DAD1 at the edges of the neural plate causes a small reduction in the incidence of PCD compared to electroporated controls in some embryos, but this is quite variable.…”

Section: Discussionmentioning

confidence: 99%

Regulation of programmed cell death during neural induction in the chick embryo

Gibson

Robinson²,

Streit³

et al. 2011

Int. J. Dev. Biol.

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To study early responses to neural inducing signals from the organizer (Hensen's node), a differential screen was performed in primitive streak stage chick embryos, comparing cells that had or had not been exposed to a node graft for 5 hours. Three of the genes isolated have been implicated in Programmed Cell Death (PCD): Defender Against Cell Death (Dad1), Polyubiquitin II (UbII) and Ferritin Heavy chain (fth1). We therefore explored the potential involvement of PCD in neural induction. Dad1, UbII and fth1 are expressed in partly overlapping domains during early neural plate development, along with the pro-apoptotic gene Cas9 and the death effector Cas3. Dad1 and UbII are induced by a node graft within 3 hours. TUNEL staining revealed that PCD is initially random, but both during normal development and following neural induction by a grafted node, it becomes concentrated at the border of the forming neural plate and anterior non-neural ectoderm and downregulated from the neural plate itself. PCD was observed in regions of Caspase expression that are free from Dad1, consistent with the known anti-apoptotic role of Dad1. However, gain-and loss-of-function of any of these genes had no detectable effect on cell identity or on neural plate development. This study reveals that early development of the neural plate is accompanied by induction of putative pro-and anti-apoptotic genes in distinct domains. We suggest that the neural plate is protected against apoptosis, confining cell death to its border and adjacent non-neural ectoderm.

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Section: Discussionmentioning

confidence: 99%

Regulation of programmed cell death during neural induction in the chick embryo

Gibson

Robinson²,

Streit³

et al. 2011

Int. J. Dev. Biol.

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“…The early chick and mouse embryos also show cell death, often with apoptotic morphology, during gastrulation (Jacobson 1938;Bellairs 1961;Daniel and Olson 1966;Sanders et al 1997); neural tube closure (Schlüter 1973;Geelen and Langman 1977); neural crest formation (Vermeij-Keers and Poelmann 1980;Lumsden et al 1991;Homma et al 1994), and among the primordial germ cells (Coucouvanis et al 1993;Pesce and De Felici 1994). In the mouse, cell death has been described both in the ectoderm (Poelmann and Vermeij-Keers 1976;Poelmann 1980;Chen et al 1994) and in the visceral endoderm from the mid-streak stage onwards (Lawson et al 1986;Lawson and Pederson 1987), but its significance has been enigmatic.…”

Section: Introductionmentioning

confidence: 98%

Patterns of cell death during gastrulation in chick and mouse embryos

Sanders

Torkkeli

French

1997

Anatomy and Embryology

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We have examined the distribution of cells at an early stage of the cell death process in gastrulating chick and mouse embryos, using a DNA nick end-labelling technique to label nuclei that are undergoing DNA fragmentation in situ. In the chick embryo, the incidence of nuclei showing DNA fragmentation was mapped by digitizing the occurrence of these nuclei from sections, and reconstructing the three separate layers of the entire embryo at several stages of gastrulation. In the chick, DNA fragmentation was found in nuclei throughout the embryo, in cells of all three germ layers, but most especially in the epiblast in the rostral germinal crescent and in the lateral marginal zones. This region of greatest cell death formed an arc rostrally and laterally in the epiblast, and was consistent through gastrulation and into the early neurulation stage. While the extensive cell death in the chick embryo may be due to cell redundancy, it is also possible that the pattern of death observed could be related to the compression of the embryo against the barrier of yolk at the periphery of the area pellucida during expansion. In a number of cases in the chick, local regions of elevated cell death were also observed in the primitive streak. This may be associated with the changing cell-cell and cell-matrix interactions experienced by cells traversing the primitive streak. In the gastrulating mouse embryo, by contrast, nuclei undergoing DNA fragmentation showed no consistent regions of elevated incidence, in any of the embryonic layers. DNA fragmentation in these embryos was, however, observed in nuclei of cells in the visceral endoderm and in the epiblast. The lack of any clear pattern of DNA fragmentation in the mouse embryo at this stage of development leaves the roles of the dying cells enigmatic. The death may, however, be lineage-related or be a reflection of a cellular redundancy necessary in a developing system that is undergoing extensive cell rearrangement and cellular adhesive change.

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“…Although the mechanisms of protection against apoptosis by bcl-2 are not fully understood, it apparently plays a role in the regulation of pore opening of mitochondria (Zamzami et al, 1996), and in protection against oxidative damage (Hockenbery et al, 1993). Using immunohistochemistry, Sanders et al (1997b) found that bcl-2 was distributed throughout the gastrulating (stage 4) chick embryo. In the present study, we found that bcl-2 is expressed at earlier developmental stages as well.…”

Section: Blastodermal Cells Demonstrate Resistance To Temperature Shocksmentioning

confidence: 99%

“…Bcl-2, sharing sequence and functional similarities with ced-9, has been detected as early as stage E8.5 in mouse embryos and by E10.5 is prominent in the immature neural tissue of the brain and spinal cord (Novak and Korsmeyer, 1994). More recently, the bcl-2 and bax proteins were detected in sections of stage 4-5 (gastrulation) chick embryos immunostained for these antigens (Sanders et al, 1997b). Although c-myc is expressed in all proliferating cells, and promotes apoptosis under certain circumstances, its role as a potential cell death regulatory gene in pre-gastrulating embryos has not been explored.…”

Section: Introductionmentioning

confidence: 99%

Cell death in the avian blastoderm: resistance to stress-induced apoptosis and expression of anti-apoptotic genes

et al. 1998

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We investigated the expression of an apoptotic cell death program in blastodermal cells prior to gastrulation and the susceptibility of these cells to stress-induced cell death. A low frequency (3.1%) of apoptotic blastodermal cells was observed in Hoechst 33342-vitally stained cytological preparations of complete blastoderms from unincubated eggs. These cells showed the stereotypic features of apoptosis includingaprogressionofnuclearchanges,cellshrinkageand blebbing, and the formation of apoptotic bodies. Prolonged storage of eggs at 128C induced apoptosis in blastodermal cells (14%). A modest amount of apoptosis (10%) was also induced at the heat shock temperature of 488C, but not at 458C. Etoposide and other potent cytotoxic drugs failed to induce apoptosis in the blastodermal cells after 4 h of exposure. Progressively more apoptosis was induced at 8 and 24 h, but it did not exceed 35% of the cells. We detected transcripts for the anti-apoptotic genes bcl-2, bcl-x L , and hsp70. The developmental expression of these genes, especially hsp70, correlated with the delayed and limited stress-induction of apoptosis. These studies reveal the capacity of pre-streak blastodermal cells to engage in apoptosis and their relative resistance to stress conditions. This may be due to the prominent expression of hsp70 and/or multiple cell death genes which primarily antagonize cell death.

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Cell death in the gastrulating chick embryo: potential roles for tumor necrosis factor-alpha (TNF-α)

Cited by 11 publications

References 62 publications

Regulation of programmed cell death during neural induction in the chick embryo

Regulation of programmed cell death during neural induction in the chick embryo

Patterns of cell death during gastrulation in chick and mouse embryos

Cell death in the avian blastoderm: resistance to stress-induced apoptosis and expression of anti-apoptotic genes

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