Apoptosis in sea urchin oocytes, eggs, and early embryos

Voronina, Ekaterina; Wessel, Gary M.

doi:10.1002/mrd.1120

Cited by 53 publications

(36 citation statements)

References 16 publications

(13 reference statements)

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“…When the results of the TUNEL assay are examined it is apparent that some cells, a significantly lower percentage, are apoptotic without having been exposed to UVR. A functional apoptotic pathway has previously been shown in sea urchin embryos and larvae (Voronina and Wessel, 2001;Roccheri et al, 2002) and the results reported here for green sea urchin embryos reveal a significant increase in the number of apoptotic cells after exposure to UVR. While the work of Voronina and Wessel (2001) suggests that the TUNEL assay may underestimate the number of apoptotic cells, we feel that this underestimation would be systematic throughout our experiments and thus not affect the interpretation of UVR-induced apoptosis in the treatments described above.…”

Section: Discussionsupporting

confidence: 80%

Exposure to ultraviolet radiation causes apoptosis in developing sea urchin embryos

Lesser

Kruse

Barry

2003

Journal of Experimental Biology

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SUMMARYLaboratory exposures of embryos from the sea urchin Strongylocentrotus droebachiensis to ultraviolet B radiation (UV-B, 290-320 nm), equivalent to a depth of 1-3 m in the Gulf of Maine, resulted in significant damage to DNA measured as cyclobutane pyrimidine dimer formation. Cells with DNA damage caused by ultraviolet radiation (UVR, 290-400 nm) and oxidative stress can survive, but are often retained in the G1/S phase of the cell cycle to repair DNA as a result of the expression of cell cycle genes such as p53 and p21, and the subsequent inhibition of the activity of cyclin-dependent kinases such as cdc2; if DNA cannot be repaired it can lead to programmed cell death or apoptosis. Sea urchin embryos exposed to UV-B radiation exhibit significantly higher protein concentrations of the antioxidant enzyme superoxide dismutase, and the transcriptional activators p53 and p21. The downstream activator of the cell cycle,cdc2, showed significantly lower protein concentrations with exposure to increasingly shorter wavelengths of UVR. Decreases in cdc2 could have been caused directly by exposure to UV-B or as a result of downregulation via the p53, p21 cascade, or both. These cellular events lead to apoptosis, as shown by the significant increase in DNA strand breaks observed in the nuclei of developing embryos exposed to UVR using the TUNEL assay. Cellular death, and a decrease in sea urchin embryo survivorship,are caused by the indirect and direct effects of exposure to UVR that leads to apoptosis in these laboratory experiments.

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Section: Discussionsupporting

confidence: 80%

Exposure to ultraviolet radiation causes apoptosis in developing sea urchin embryos

Lesser

Kruse

Barry

2003

Journal of Experimental Biology

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“…Activation of caspases in sea urchins has also been reported for embryos exposed to staurosporine (Voronina and Wessel, 2001). These authors observed differences in apoptotic response between oocytes, eggs and early sea urchin embryos, suggesting that activation of apoptotic pathways may differ depending on the developmental stage.…”

Section: Discussionmentioning

confidence: 68%

A marine diatom-derived aldehyde induces apoptosis in copepod and sea urchin embryos

Romano

Russo

Buttino

et al. 2003

Journal of Experimental Biology

100

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SUMMARY The diatom-derived aldehyde 2-trans-4-trans-decadienal(DD) was tested as an apoptogenic inducer in both copepod and sea urchin embryos, using terminal-deoxynucleotidyl-transferase-mediated dUTP nick-end labelling (TUNEL), DNA fragmentation profiling (laddering) and an assay for caspase-3 activity. DD induced TUNEL positivity and DNA laddering, but not caspase-like activation, in copepod embryos spawned by females fed for 10-15 days the diatom diet Thalassiosira rotula Meunier (in vivo),or when newly spawned eggs were exposed for 1 h to 5 μg ml-1 DD(in vitro). To our knowledge, this is the first time that evidence for an apoptotic process in copepods has been obtained by cytochemical (TUNEL)and biochemical (DNA fragmentation) approaches. The absence of caspase-like activity in copepod embryos suggests that caspase-independent programmed cell death occurs in these organisms. In sea urchin embryos, DD induced apoptosis and also activated a caspase-3-like protease. The saturated aldehyde decanal induced apoptosis at higher concentrations and after a longer incubation period than DD, indicating that α,β-unsaturation of the molecule,coupled with the aldehyde group, is responsible for the greater biological activity of DD. Since diatoms are an important food source for marine herbivores such as copepods and sea urchins, these findings may help explain why unsaturated aldehydes often induce reproductive failure, with important ecological consequences at the population level.

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“…The effect on cell viability can be explained by the fact that eIF4E-binding peptides were linked to the penetratin peptide-carrier sequence, which mediates the rapid transport of peptides across cell membranes. Sea urchin eggs possess functional apoptotic machinery (Voronina and Wessel, 2001). Yet, the microinjection of 4E-BP peptide into unfertilized sea urchin eggs did not affect cell viability.…”

Section: Discussionmentioning

confidence: 99%

Embryonic-stage-dependent changes in the level of eIF4E-binding proteins during early development of sea urchin embryos

Salaün

Boulben

Mulner‐Lorillon

et al. 2005

Journal of Cell Science

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The eukaryotic initiation factor 4E (eIF4E)-binding proteins (4E-BPs) inhibit translation initiation by binding eIF4E and preventing recruitment of the translation machinery to mRNA. We have previously shown that fertilization of sea urchin eggs triggers eIF4E–4E-BP complex dissociation and 4E-BP degradation. Here, we show that microinjection of eIF4E-binding motif peptide into unfertilized eggs delays the onset of the first mitosis triggered by fertilization, demonstrating that dissociation of the eIF4E–4E-BP complex is functionally important for the first mitotic division in sea urchin embryos. We also show by gel filtration analyses that eIF4E is present in unfertilized eggs as an 80 kDa molecular mass complex containing 4E-BP and a new 4E-BP of 40 kDa. Fertilization triggers the dissociation of eIF4E from these two 4E-BPs and triggers the rapid recruitment of eIF4E into a high-molecular-mass complex. Release of eIF4E from the two 4E-BPs is correlated with a decrease in the total level of both 4E-BPs following fertilization. Abundance of the two 4E-BPs has been monitored during embryonic development. The level of the two proteins remains very low during the rapid cleavage stage of early development and increases 8 hours after fertilization. These results demonstrate that these two 4E-BPs are down- and upregulated during the embryonic development of sea urchins. Consequently, these data suggest that eIF4E availability to other partners represents an important determinant of the early development of sea urchin embryos.

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Apoptosis in sea urchin oocytes, eggs, and early embryos

Cited by 53 publications

References 16 publications

Exposure to ultraviolet radiation causes apoptosis in developing sea urchin embryos

Exposure to ultraviolet radiation causes apoptosis in developing sea urchin embryos

A marine diatom-derived aldehyde induces apoptosis in copepod and sea urchin embryos

Embryonic-stage-dependent changes in the level of eIF4E-binding proteins during early development of sea urchin embryos

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