In the fission yeast Schizosaccharomyces pombe, we have detected prominent DNA breaks that appeared shortly after premeiotic DNA replication. These breaks, like meiotic recombination, required the products of the six rec genes tested. Prominent breaks were detected at widely separated sites, about 100-300 kb apart, equivalent to about 50-150 sites per genome or approximately the number of meiotic recombination events. Certain features of these breaks are similar to those in the distantly related yeast Saccharomyces cerevisiae, the only other organism in which meiotic DNA breaks have been reported. Other features, however, appear to be different. These results suggest that, although DNA breaks may be a general feature of meiotic recombination, the breaks in S. pombe may play a role different from those in S. cerevisiae.

Meiotic recombination is initiated by DNA double-strand breaks (DSBs) made by Spo11 (Rec12 in fission yeast), which becomes covalently linked to the DSB ends. Like recombination events, DSBs occur at hotspots in the genome, but the genetic factors responsible for most hotspots have remained elusive. Here we describe in fission yeast the genome-wide distribution of meiosis-specific Rec12-DNA linkages, which closely parallel DSBs measured by conventional Southern blot hybridization. Prominent DSB hotspots are located ∼65 kb apart, separated by intervals with little or no detectable breakage. Most hotspots lie within exceptionally large intergenic regions. Thus, the chromosomal architecture responsible for hotspots in fission yeast is markedly different from that of budding yeast, in which DSB hotspots are much more closely spaced and, in many regions of the genome, occur at each promoter. Our analysis in fission yeast reveals a clearly identifiable chromosomal feature that can predict the majority of recombination hotspots across a whole genome and provides a basis for searching for the chromosomal features that dictate hotspots of meiotic recombination in other organisms, including humans.

Position-effect variegation is the inactivation in some cells of a gene translocated next to heterochromatin, the region of the chromosome that is permanently condensed. The number of copies of the Drosophila gene Suvar(3)7 is a dose-limiting factor in this phenomenon, and seems from its sequence that it encodes a protein with five widely spaced zinc-fingers. This novel arrangement of zinc-fingers could help in packaging the chromatin fibre into heterochromatin, and also reflect a novel method of controlling the expression from DNA domains.

The PsaF polypeptide of photosystem I (PSI) is located on the lumen side of the thylakoid membrane and its precise role is not yet fully understood. Here we describe the isolation of a psaF‐deficient mutant of the green alga Chlamydomonas reinhardtii generated by co‐transforming the nuclear genome of the cw15‐arg7A strain with two plasmids: one harboring a mutated version of the psaF gene and the other containing the argininosuccinate lyase gene conferring arginine prototrophy. This psaF mutant still assembles a functional PSI complex and is capable of photoautotrophic growth. However, electron transfer from plastocyanin to P700+, the oxidized reaction center chlorophyll dimer, is dramatically reduced in the mutant, indicating that the PsaF subunit plays an important role in docking plastocyanin to the PSI complex. These results contrast with those obtained previously with a cyanobacterial psaF‐, psaJ‐ double mutant where no phenotype was apparent.