Abstract

THE hypotheses attempting to explain the mechanism of mosaic formation in cases of mosaicism caused by eversporting displacements fall into two groups. According to the hypotheses of the first group, the original chromosome aberration, peculiar to the given mosaic strain, causes the occurrence in somatic cells of secondary changes in the chromosome structure, such as the losses of chromosome pieces (Patterson, 1932; Schultz, 1936), the changes of the size of laterally attached translocated pieces (Stern, 1935), or the occurrence of gene mutations (Sidorov, 1936; 1940; 1941; Demerec and Slizinska, 1937). According to all these hypotheses a mosaic organism is considered a chimera. The alternative point of view is expressed in the hypotheses of the second group, all of which explain mosaicism in terms of position effect, either the interchromosomal (Muller, 1935; Ssacharov, 1936) or intrachromosomal (Dubinin, 1936; Belgovsky, 1938; Prokofyeva-Belgovskaya, 1939a, 1939b; Panshin, 1938; Khvostova, 1939) one. According to this point of view, the somatic cells of a mosaic organism are all genotypically alike, the differences in characters they display depending solely upon the differences in biochemical reactions taking place in the immediate vicinity of genes responsible for mosaicism. In 1938 I suggested that mosaicism of the type under discussion is to be ascribed chiefly to two causes: (1) the weakening of the biochemical efficiency of the gene primarily responsible for mosaicism, this weakening resulting from the interaction of substances produced by the ISO

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