Abstract

That ultraviolet-induced respiratory deficiency in Saccharomyces was photoreversible implicated the nucleus as the site of radiation damage; further, the fact that only the induction of variants in respiration adapted cells was photoreversible supported the primary conclusion drawn from this work that the induction of respiration deficiency resulted from damage to a nuclear entity involved in the adaptive formation of respiratory enzymes. Unlike the photoreactivation of induced respiration deficient variants, photoreactivation of inactivational damage was independent of the state of cellular adaptation to respiration. This, together with the observation that the expression of ultraviolet damage resulting in the production of respiration deficient variants was completely determined by post-irradiation respiratory conditions while the expression of inactivational damage was only partly so determined, revealed that cellular inactivation and the induction of respiratory variants involve different nuclear disturbances.This paper presents the first experimental challenge to the hitherto accepted concept that non-segregational, respiratory deficiency in Saccharomyces is cytoplasmically inherited.

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