p53-Independent checkpoint controls in a plant cell model

Abstract

Allium cepa L. meristems were used as a plant model to study the p53-independent control of S and G2 phases by checkpoint pathways, in eukaryotic cells. Checkpoint blocks were induced at early and mid S by hydroxyurea. After their spontaneous override, cells became accumulated in G2-prophase, giving rise later on to a delayed mitotic wave. Cell growth was maintained during the checkpoint blocks, as the delayed mitoses were larger in size than the control ones. Under continuous hydroxyurea treatment, the delayed mitotic was formed by two subpopulations: normal mitoses corresponding to cells having properly recovered from the checkpoint block, and abnormal ones resulting from checkpoint adaptation. These latter cells displayed broken chromatids as they had unduly overriden the G2 checkpoint block, without completing DNA repair. The frequency of the checkpointadapted mitoses increased with the hydroxyurea concentration from 0.25 to 1.0 mM. However, from 1 mM hydroxyurea upwards, some of the cells lost their competence for checkpoint adaptation. Therefore, the dose of a genotoxic agent that still allows G2 checkpoint adaptation should always be applied in order to get rid of uncontrolled proliferating cells. This is specially suitable for cells lacking a functional p53 protein.

Increased transcription in hydroxyurea-treated root meristem cells of Vicia faba

“…Occurrence of micronuclei indicated that some cells still continued cell cycle progression and preserved the ability to enter aberrant mitotic division in spite of blocked or slowed down DNA replication (data not shown). Moreover, cells of Allium cepa blocked by an intra-S checkpoint, activated in response to HU, were able to complete both their DNA synthesis and post-replication repair (Pelayo et al 2003).

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Assessment of antimitotic and programmed cell death stimulation potentials of Galium sinaicum (Delile ex Decne) Boiss. at cellular level

“…So, the data in the present study confirm that both entry into and exit from mitosis is blocked in treated cells suggesting that GsEE may interfere with the balance between cyclin condensation required for entry into mitosis and exit from mitosis. Pelayo et al (2003) declared that plant cells unable to perform checkpoint adaptation may instead induce a program of cell death or may simply fail to proliferate, remaining inactive in mitosis depending on the stimulus and features of cell damage.…”