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. 2022 Jan 1;36(1-2):53–69. doi: 10.1101/gad.348973.121

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© 2022 Pyatnitskaya et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 5. — Forcing the interaction between Ecm11 and Zip4 is sufficient to restore both Gmc2 recruitment to chromosomes and synaptonemal complex assembly. (A) Strategy to tether Ecm11LLDD fused to the FRB domain to Zip4 fused to the Fkpb12 domain by addition of rapamycin. (B) Meiotic progression as assessed by DAPI staining of nuclei to monitor meiotic divisions, with (+rapamycin) and without (−rapamycin) 1 µM rapamycin added at 3.5 h after meiotic induction. (C) Gmc2 localization on surface-spread chromosomes. Pachytene-stage nuclei are shown. (Red) Gmc2, (green) anti-Red1, (blue) DAPI. (D) Zip1 localization on surface-spread chromosomes. Pachytene-stage nuclei are shown. (Green) Anti-Zip1, (blue) DAPI. (E, top) Quantification of Zip1 intensity observed in D. (Bottom) Quantification of polycomplex areas observed in D. Numbers of spreads are indicated for each condition. (****) P-value < 0.0001, Wilcoxon test.