A heritable structural alteration of the yeast mitochondrion.
Prions have revived interest in hereditary change that is due to change in cellular structure. How pervasive is structural inheritance and what are its mechanisms? Described here is the initial characterization of [Leu(P)], a heritable structural change of the mitochondrion of Saccharomyces cerevisiae that often but not always accompanies the loss of all or part of the mitochondrial genome. Three phenotypes are reported in [Leu(P)] vs. [Leu(+)] strains: twofold slower growth, threefold slower growth in the absence of leucine, and a marked delocalization of nuclear-encoded protein destined for the mitochondrion. Introduction of mitochondria from a [Leu(+)] strain by cytoduction can convert a [Leu(P)] strain to [Leu(+)] and vice versa. Evidence against the Mendelian inheritance of the trait is presented. The incomplete dominance of [Leu(P)] and [Leu(+)] and the failure of HSP104 deletion to have any effect suggest that the trait is not specified by a prion but instead represents a new class of heritable structural change.
Department of Genetics, University of Washington, Seattle, Washington 98195, USA. lockshon@u.washington.edu
Daniel
D
Lockshon
D006360:Heat-Shock Proteins / Q000235:genetics; D007930:Leucine / Q000378:metabolism*; D008928:Mitochondria / Q000235:genetics*; D011328:Prions / Q000235:genetics; D012441:Saccharomyces cerevisiae / Q000235:genetics* / Q000378:metabolism / Q000648:ultrastructure; D029701:Saccharomyces cerevisiae Proteins / Q000235:genetics
D006360:Heat-Shock Proteins; D011328:Prions; D029701:Saccharomyces cerevisiae Proteins; C070972:HsP104 protein, S cerevisiae; D007930:Leucine