Deoxyribonucleic Acid Replication of Somatic Cells in the Chinese Hamster

Abstract

OVER the past few years increasing attention has been focused on the relationship of gene inactivation to the phenomena of interphase DNA condensation and late DNA replication. It has been shown that the sex chromatin body of female mammalian cells appears during early embryogenesis¹ and is composed of one X chromosome². In 1961 Lyon postulated that phenotypic variegation in heterozygotic female mice was a consequence of the inactivation of either the maternal or paternal X chromosome³. As well as being mostly metabolically inert, this X chromosome replicates late in the DNA synthetic period^4,5. It has been assumed that the Y chromosome also becomes largely inactivated during early embryonic life, since it shows positive heteropyknosis in early prophase, is late replicating, and extra Y chromosomes produce no conspicuous phenotypic effects⁶. That late-replicating autosomal DNA may be related to gene inactivation is supported by the observation that the abnormal chromosome material found in most human autosomal chromosome abnormalities replicates toward the end of the DNA synthetic period. It was postulated that this late-replicating DNA is less deleterious than early replicating DNA when present in excess or deleted because it is relatively inert⁶. Furthermore, it has been shown that interphase heterochromatin is less active than euchromatin in that it produces less RNA^7,8, and that late-replicating chromosomes have less capacity for RNA synthesis⁹.