Skp1 together with Fbh1 resolves meiotic recombination intermediates.

<p>(<b>A</b>) Temperature sensitivity of the <i>skp1-a7</i> mutant was partially suppressed by overexpression of Fbh1 from the plasmid vector pREP1. Ten-fold serial dilution of the indicated strains was spotted on minimal media with or without thiamine and then incubated at 25°C and 36°C. Overexpression is induced on the medium without thiamine (−thiamine). (<b>B</b>) Growth defects of <i>skp1-a7</i> and <i>fbh1</i>Δ mutants were suppressed by <i>rad3</i>Δ, removal of the Rad3-dependent DNA damage checkpoint. (<b>C, D</b>) Frequency of the normal and bent spindle in mitosis (C) and the aberrant ‘crossing’ spindles in MII (D) in the indicated strains. <i>n</i>≥30. (<b>E</b>) Schematic diagram for Fbh1 WT and Fbh1-D485N (the helicase-dead form), Fbh1-L14A P15A and Fbh1-P15A L26A (the F-box-deficient form) mutant proteins. (<b>F</b>) Sensitivity to 5 µM CPT (camptothecin) was tested for the indicated strains. (<b>G</b>) <i>fbh1-D485N</i> and <i>fbh1-P15A L26A</i> mutants exhibited the bent-spindle phenotype, whereas <i>fbh1-L14A P15A</i> did not. GFP-Atb2 in MI of the indicated strains is shown. Bars, 5 µm.