Melee. gen. Genet. 123, 143--158 (1973) © by Springer-Verlag 1973 On a Possible Correlation between Fine-Structure Map Expansion and Reciprocal Recombination Based on Crossing-0ver A. Ahmad and U. Leupold Institute of General Microbiology,University of Bern, Switzerland Received February 28, 1973 Summary. A possible alternative explanation of the map expansion observed in fungal fine-structure maps is presented. It does not rely on independent correction of base-pair mismatches in hybrid-DNA segments (Holliday, 1968; Fincham and Holliday, 1970) but on the contribution of reciprocal crossing-over to the total frequency of recombination. Within the frame of a modified fixed pairing region model chosen for discussion, this contribution is expected to increase with the square of the distance between the mutant sites of a two-point cross if the pairs of single-strand breaks serving for hybrid-Dk~Aformation are assumed to be distributed at random within the fixed pairing region. In combination with a general marker effect which reduces the non-reciprocal but not the reciprocal contribution to recombination, this will lead to map expansion. Introduction Current models of recombination can be divided into two broad categories: 1. Those relying on breakage of DNA strands and formation of hybrid-DNA by reunion, followed by correction of mismatches in the hybrid-regions (White- house, 1963; Holliday, 1964; Meselson, 1964). 2. The fixed pairing region (FPR) models (Murray, 1961 ; Stab], 1961). Present models of this type do not rely on correction of mismatches to explain recombinant formation. According to these FPR models, some form of breakage and copy mechanism is responsible for genetic recombination. Recent contributions in this series came from Stahl (1969), Boon and Zinder (1969) and Paszewski (1970). It is not necessary to go L~to a detailed discussion of present models of the FPR type, as this was recently done by Holliday and Whitehouse (1970). Perhaps it will suffice to point out that Stahl's model explains conversion by postulating two non- reciprocal exchanges in segments of chromosomes that have undergone an extra duplication. Conversion would occur in the region between the two exchanges. However, these ideas are not able to explain some of the important features of observed eukaryotic recombination data, such as the map expansion which is regularly observed in fungal fine-structure maps based on meiotic recombination (Holliday, 1968; Fincham and Holliday, 1970). Assuming that ends of fixed pairing regions coincide with gene ends, Holliday and Whitehouse have pointed out that Stahl's model also fails to explain the data on polarity in recombination. On Stahl's model, the mutants in the middle of the FPI~ (and therefore in the middle of a gene, if FPR ends coincide with gene ends) are expected to show dominant polarity in crosses to mutants towards the ends of the FPR. Within genes, this type of polarisation has not been observed. The 10 Melee. gem Genet. 123