Abstract

Taken altogether, the EM evidence we have obtained indicates that the induced (both viral and PEG) and spontaneous (entrance of a splenocyte into a cell) fusion of mammalian somatic cells are associated with alterations in the structure of fusing cells. For example there are alterations in the structure of not only the surfaces of fusing cells but also in the nucleus envelopes and cytoplasmic organelles after PEG treatment. Also, there is long retention of cellular plasma membrane remnants in virally-induced heterokaryons. In short, for each case the alterations were unquestionably specific, in response to the imposed challenge. These specific features not only determine the efficiency and rate of fusion, but also the mode of which the hybrid nucleus is formed. This mode directly determines the fate of the synkaryon and the stability of the so formed hybrid genome. It might be thought that an increase in the inner nuclear envelope observed in some hybrids would counteract the consequences of the disproportion arising between the increase in cell volume and nuclear surface. The finger-like invaginations of the hybrid nuclei nuclear envelope, surrounded by replicatively and transcriptionally active chromatin, appear to be EM demonstrations of such counteracting mechanisms. These invaginations, by augmenting the available inner layer, most likely increase the anchorage sites for chromatin. It is noteworthy that the invaginations occur mainly in multichromosomal hybrids with little chromosome loss. It appears possible that some of the hybrids may contain particular chromosomes from the more differentiated parent cell.

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