2005
DOI: 10.1002/dvdy.20449
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Chk2/Cds1 protein kinase blocks apoptosis during early development of Xenopus laevis

Abstract: Early Xenopus laevis embryos possess cell cycles that do not arrest at checkpoints in response to damaged DNA. At the midblastula transition (MBT), embryos with damaged DNA undergo apoptosis. After the MBT, DNA damage triggers cell cycle arrest rather than apoptosis. The transition from checkpoint-unregulated to checkpoint-regulated cycles makes Xenopus embryos compelling for studying mechanisms regulating response to genomic damage. The DNA damage checkpoint is mediated by the Chk2/Cds1 kinase. Conflicting ev… Show more

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Cited by 11 publications
(20 citation statements)
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“…If Chk1 was inhibited, the development was normal until the onset of gastrulation at which the embryo died, with cells entering in apoptosis. In zygotes with two blastomeres injected with SAMDL mRNAs, apoptosis was also observed at gastrulation [21,22]. If these mRNAs were injected on a side only in embryos with 4 to 8 cells, a large number of animals became tadpoles; if embryos were 16 to 32 cells, all individuals became tadpoles with sometimes abnormalities.…”
Section: Regulation Of Apoptosis During Segmentation and Gastrulationmentioning
confidence: 99%
“…If Chk1 was inhibited, the development was normal until the onset of gastrulation at which the embryo died, with cells entering in apoptosis. In zygotes with two blastomeres injected with SAMDL mRNAs, apoptosis was also observed at gastrulation [21,22]. If these mRNAs were injected on a side only in embryos with 4 to 8 cells, a large number of animals became tadpoles; if embryos were 16 to 32 cells, all individuals became tadpoles with sometimes abnormalities.…”
Section: Regulation Of Apoptosis During Segmentation and Gastrulationmentioning
confidence: 99%
“…Our studies in which we microinject cytochrome c into individual blastomeres and cause entire embryo apoptosis support this idea. It is well known that checkpoint activation does not occur in embryos until after the mid-blastula transition36; one important reason for such a delay might be to prevent the triggering of apoptosis by minor cellular damage during a time when death of an individual blastomere would lead to death of the entire embryo. Conversely, in the presence of a cell-damaging stimulus sufficiently strong to warrant induction of cell death in a single cell, it would likely be advantageous to rapidly induce death of the entire embryo to avoid significant developmental anomalies.…”
Section: Discussionmentioning
confidence: 99%
“…Thus, in this Xenopus embryonic system, SAMDC-overexpressed cells underwent apoptosis, rather than arresting cell cycles. This is interesting, since adult-type cells that happened to have DNA damages by γ-ray irradiation usually arrest cell cycles rather than undergoing apoptosis (Wroble and Sible, 2005). …”
Section: The Cell Dissociation Observed Was Due To Execution Of Apoptmentioning
confidence: 99%
“…Furthermore, onset of the cell dissociation executed by γ-ray exposure has been shown to be suppressed “partially” (the onset of the cell dissociation was postponed only by 2–3 hrs) by prior microinjection of Bcl-2 mRNA (Anderson et al 1997; Hensey and Gautier, 1997). In more recent studies on the apoptosis induced by DNA-damaging agent like γ-ray, cyclin-dependent protein kinases have been shown to play important roles to switch on the apoptosis (Finkielstein et al 2002; Carter and Sible, 2003; Carter et al 2006; Wroble and Sible, 2005). …”
Section: Various Toxic Treatments Other Than Samdc Overexpression Indmentioning
confidence: 99%
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