The effective site of the lesion resulting from a trichocyst non-discharge stable differentiation of somatic nuclei in Paramecium tetraurelia.

Previous work has shown in Paramecium tetraurelia that recessive genie mutants with the phenotype N, non-discharge of trichocysts from intact cells in response to a standard test (exposure to tannic or picric acid), are in some mutants due to lesions in trichocyst development and in others due to lesions in the cytoplasm; and that in stock di /J the same homozygous germinal genotype can yield by stable differentiation of somatic nuclei both N clones and D (discharge) clones. The site of the lesion in the N clones of dnj was investigated by the same microinjection protocol used earlier for analysis of the genie mutants: cytoplasm containing trichocysts was removed from wild-type (D) and from dii3 (N) cells and injected into cells of both dii3 (N) and the genie mutant ft A (normal cytoplasm, but morphologically abnormal trichocysts incapable of insertion in the cell cortex or of discharge from intact cells). Trichocysts from each donor behaved the same in both recipients: trichocysts from D cells could discharge; those from dii3 N cells could not. Thus, the cytoplasm of rf//j (N) cells does not prevent the discharge of trichocysts from D cells and the trichocysts from dii3 (N) cells cannot discharge \nftA cells in which trichocysts from wild-type (D) cells can. It appears, therefore, that the lesion in di 13 (N) cells, due to a stable differentiation of somatic nuclei, is in the trichocysts themselves, as it is in certain genie mutants.