Structural Inheritance in Yeast

University Of Washington, Seattle WA

Investigators

Abstract

The genome is not the sole determinant of heredity. This was demonstrated decades ago in the ciliated protoza and more recently with the discovery of prions in mammals and fungi. These are examples of a rare phenomenon or of a signifgicant aspect of biology that needs to be more widely explored. The molecular mechanism of the prion type of structural inheritance is becoming clear, yet cortical inheritance in the ciliates and other phenomena suggest that there may be a number of ways that structures act as their own templates to transmit heritable information. The proposed work will explore the molecular basis of a new example of a structurally inherited trait in yeast. The two most significant phenotypes of strains bearing this trait, called [leu], are a three-fold slower growth rate in the absence of leucine, and the failure of a large amount of mitochondrially-targeted protein to be localized to the organelle. Several lines of evidence argue that [leu] is not the result of a nuclear change. The self-templated inheritance of [leu] also is not due to a change in the mitochondrial genome, because rho-minus strains lacking mitochondrial DNS can be either [leu] or [LEU]. Additional experiments lend support to the hypothesis that [leu] is caused by some alteration of the mitochondrial structure itself. The goal of the proposed work is to gain additional evidence for or against the hypothesis that [leu] has a nuclear mechanism of inheritance. If experiments rule out a nuclear role for [leu] inheritance, the path is open for additional studies to determine the molecular mechanism of [leu] inheritance.