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. 2021 Jul 1;49(13):7537–7553. doi: 10.1093/nar/gkab566

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© The Author(s) 2021. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Figure 7. — Roles of the EG complex in a feedback mechanism linked to DSB number and ZMM-dependent CO formation. (A) Proposed mechanism of chromosome synapsis-dependent feedback based on ecm11 and gmc2 mutant phenotypes. The EG complex facilitates Zip1 chromosomal assembly (45) and modulates the meiotic recombination frequency and distribution through chromosome synapsis-dependent feedback. Delay of JM resolution in the absence of the EG complex may be explained by a pathway in which unstable SC structures cause defective CO-fated recombination. The SC central region provides an environment for correct recombination processing through phase separation. (B) Model of the roles of the EG complex in feedback control of DSB formation and the ZMM-dependent crossover pathway.