Figure 7.

Two models for the formation of long gene conversion tracts that are unassociated with crossovers. The data that require explanation are (1) crossover-associated conversion events are shorter in the exo1 strain than in wild type and (2) crossover-unassociated conversions are longer than crossover-associated conversions in the exo1 strain. The labels are the same as in Figure 6. The observations can be explained by an oversynthesis model (A and B) or by a BIR model (C and D). (A) UV-induced conversion in the wild-type strain (oversynthesis model). The synthesis from the invading strand is more extensive than the amount of DNA resected in the NCO pathway. The reinvasion during SDSA displaces the 5′ end of invaded homolog, and the resulting single-stranded branch is removed (shown by a triangle). In the CO pathway, the heteroduplex region is limited by resection. (B) UV-induced conversion in the exo1 strain (oversynthesis model). The conversion tract in the NCO pathway is similar to that observed in wild type, whereas the conversion tract for the CO pathway is shorter due to less resection. (C) UV-induced conversion in the wild-type strain (BIR model). In the NCO pathway, the conversion is a consequence of BIR. Following copying of the red chromosome, the invasion is reversed, and the end generated by BIR reassociates with the broken black chromosome. In this model, the conversion tract is not a consequence of repair of mismatches in a heteroduplex. The conversion events in the CO pathway occur by the same mechanism as in A and B. (D) UV-induced conversion in the exo1 strain (BIR model). As in C, the BIR event generating the conversion tract in the NCO pathway is not limited by resection, unlike the conversion tract in the CO pathway.