Figure 4 .

Model for role of axial element in promoting interhomolog recombination bias. (Top) DSBs occur during leptonema. In yeast it is thought that DSBs are dependent upon AE formation, in part because mutations of AE proteins such as Red1 and Hop1 decrease DSB levels (Zickler and Kleckner 1999). However, the temporal relationship is not clear in mice because RAD51/DMC1 foci (surrogates of DSBs) appear concurrent to and colocalize with AE components. Nevertheless, numerous immunocytological studies show that the DSB ends become localized to the AE cores. RAD51 and DMC1 foci in normal meiosis also colocalize to nascent AEs and HORMADs in leptonema (Barlow et al. 1997; Wojtasz et al. 2009) and actually directly interact with SYCP3 (Tarsounas et al. 1999). (Bottom) Localization of SYCP2 is dependent upon SYCP3, so as indicated, loss of SYCP3 results in aberrant pseudoaxial elements, or cores, consisting only of cohesin proteins such as REC8, SMC1β, and STAG3 (Pelttari et al. 2001; Fukuda et al. 2010). In our model, the disrupted AE structure caused by SYCP2/SYCP3 absence, which also causes discontinuities in the cohesin complex (dashed red line) allows the RAD51-bound DSB ends (depicted here in Dmc1 mutants) to have unimpeded access to the sister and will recombine in a RAD54-dependent manner. See text for more details.