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Syndrome of the Failure to Turn off Mitotic Activity in Tetrahymena thermophila: In cdaA1 Phenotypes
並列摘要
During early micronuclear mitosis of a wild type Tetrahymena thermophila, basal body proliferation and cortical growth are localized in the equatorial region of the pre-dividing cell. These processes are arrested prior to cytokinesis when the fission line gaps appear in ciliary rows. Then a putative marker of cellular polarity, the fenestrin antigen, appears in the apical zone of the dividing cell and around the old oral apparatus (OA1) and in the cortex localized posterior to the fission line gaps and around the new oral apparatus (OA2) i.e. in the apical cortex of the prospective posterior daughter cell. Prior to cytokinesis, the membranelles within OA1 and OA2 oral apparatuses are strongly labeled with the MPM2 antibody against mitotic phosphoproteins. The transition to cytokinesis is correlated with disappearance of both the polar fenestrin staining and of the phosphoprotein antigens in OA1 and OA2. cdaA1 (cell division arrest) mutant cells grown at the restrictive temperature do not produce a fission line and they do not undergo cytokinesis thereby generating irregular chains. The cdaA1 phenotypes continue elongation of their ciliary rows in equatorial regions, mostly without formation of the fission line gaps, accompanied with repetitive micronuclear mitoses and repetitive formation of the defective oral structures. In cdaA1 cells at restrictive temperature, the fenestrin antigen was recruited and then permanently found in the apical regions and around all oral apparatuses, and was always absent in equatorial regions, in spite of variability of immunostaining patterns, sizes and advancement of organization of OAs in different specimens of the same sample. The MPM2- tagged phosphoproteins were retained in all oral apparatuses in different cdaA 1 phenotypes. We suggest that the cdaA1 phenotypes produced at restrictive temperature behave as cells trapped in a metastable phase with a syndrome of an arrest of the mechanism required to regain the morphostatic stage of a non-dividing cell.