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. 2015 Oct 26;211(2):233–242. doi: 10.1083/jcb.201409035

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© 2015 Bohr et al.

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Figure 3. — Loss of MAD-1, MAD-2, or BUB-3 suppresses the synapsis defects in dynein mutants. (A) Images of germlines from wild-type, dhc-1;dlc-1^RNAi, mad-1(cd);dhc-1;dlc-1^RNAi, mad-2Δ;dhc-1;dlc-1^RNAi, bub-3Δ;dhc-1;dlc-1^RNAi;dlc-1^RNAi, mad-1(cd);dlc-1^RNAi, mad-2Δ;dlc-1^RNAi, bub-3Δ;dlc-1^RNAi, and sun-1;dlc-1^RNAi mutants stained to visualize SYP-1 and HTP-3. Regions of asynapsis are indicated by yellow dashed lines, and regions of normal synapsis are indicated by white dashed lines. Bar, 30 µm. (B) Schematic of the possible role of the APC in regulating synapsis. (C) mad-1(cd), mad-1Δ, mad-2Δ, or bub-3Δ suppresses the synapsis defect in dhc-1;dlc-1^RNAi germlines. Mutation of mat-3 does not affect synapsis in mad-1Δ;dhc-1;dlc-1^RNAi or bub-3Δ;dhc-1;dlc-1^RNAi mutants. (D) mad-1(cd), mad-2Δ, or bub-3Δ suppresses the synapsis defect in dlc-1^RNAi germlines. Error bars represent 95% confidence intervals. *, P < 0.01; **, P < 0.0001 in all graphs.