In "S. pombe", a mutant defective in the "spo11" homolog "Rec12" is deficient in meiotic recombination. However recombination can be restored to near normal levels by a deletion in "rad2", a gene that encodes an endonuclease involved in Okazaki fragment processing (Farah et al., 2005). Both crossover and non-crossover recombination were increased but double-strand breaks were undetectable. On the basis of the biochemical properties of the rad2 deletion, it was proposed that meiotic recombination can be initiated by DNA lesions other than double-strand breaks, such as nicks and gaps which accumulate during premeiotic DNA replication when Okasaki fragment processing is deficient.