Genetic control of mitosis: Is protein MAST ν40 an element of the checkpoint system?

L. I. Lebedeva, S. A. Fedorova

Research output: Contribution to journalArticlepeer-review

2 Citations (Scopus)

Abstract

The effect of the mast v40 mutation was studied using neural ganglion cells of third-instar larvae of Drosophila melanogaster. The distributions of the cells by the interphase nucleus diameter and by the distance between the sister chromosome sets in anaphase were analyzed. Three following types of defects induced by the mutation were described: (1) Monopolar mitosis or, in the case of bipolar mitosis, an abnormally short distance between the sister chromosome sets in anaphase and early telophase. We suppose that these abnormalities are caused by damage of the start and (or) motor mechanisms of centrosome separation at the beginning and in the end of mitosis. (2) Lagging and bridging of chromosomes in anaphase and early telophase. These defects seem to be related to the disruption of functioning of mitotic spindle microtubules and (or) their defective attachment to the appropriate kinetochores. (3) Unlimited division of aneuploid and polyploid cells, which may be explained either by inactivation of the checkpoint system controlling the genome ploidy or by checkpoint adaptation. Taken collectively, our results and literature data suggest that the MAST protein is an element of the checkpoint system and that division of aneuploid and polyploid cells results from inactivation of the checkpoints.

Original languageEnglish
Pages (from-to)387-392
Number of pages6
JournalRussian Journal of Genetics
Volume40
Issue number4
DOIs
Publication statusPublished - Apr 2004
Externally publishedYes

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