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Abstract: The transfer of organelle nucleic acid to the nucleus has been observed in both plants and animals. Using a unique assay to monitor mitochondrial DNA escape to the nucleus in the yeast Saccharomyces cerevisiae, we previously showed that mutations in several nuclear genes, collectively called yme mutants, cause a high rate of mitochondrial DNA escape to the nucleus. Here we demonstrate that mtDNA escape occurs via an intracellular mechanism that is dependent on the composition of the growth medium and the genetic state of the mitochondrial genome, and is independent of an RNA intermediate. Isolation of several unique second-site suppressors of the high rate of mitochondrial DNA-escape phenotype of yme mutants suggests that there are multiple independent pathways by which this nucleic acid transfer occurs. We also demonstrate that the presence of centromeric plasmids in the nucleus can reduce the perceived rate of DNA escape from the mitochondria. We propose that mitochondrial DNA-escape events are manifested as unstable nuclear plasmids that can interact with centromeric plasmids resulting in a decrease in the number of observed events.

The proteolytically defined Z‐DNA binding domain Za of human adenosine deaminase type 1 (hADAR1) has been crystallized in complex with the DNA oligomer d(TCGCGCG). The crystals were obtained from a solution containing ammonium sulfate as precipitating agent and belong to the tetragonal space group P4212. A complete diffraction data set has been collected to a resolution of 2.4 Å. The unit‐cell dimensions are a= b= 85.9, c= 71.3 Å. A Raman spectrum of the complex indicates that the DNA in the complex adopts the left‐handed Z conformation.