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. 2014 Feb 18;9(2):e89399. doi: 10.1371/journal.pone.0089399

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© 2014 Makrantoni et al

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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(A) Wild-type SLI15 (VMY194), sli15-20A (VMY162), and sli15-20D (VMY191) strains expressing Pds1-myc ₁₈ were arrested in G₁ with α-factor and synchronously released into YPD medium in the presence (+NOC) or absence (−NOC) of 30 µg/ml nocodazole. Samples were collected at the indicated times. Levels of Pds1-myc₁₈ (Pds1) and Cdc28 (loading control) were monitored by immunoblotting using anti-myc and anti-Cdc28 antibodies, respectively. (B) Wild-type pGAL-SCC1 SLI15 (VMY222), pGAL-SCC1 sli15-20A (VMY166) and pGAL-SCC1 sli15-20D (VMY356) cells expressing Pds1-myc ₁₈ were arrested with α-factor for 2 h in medium containing galactose and then released in medium containing glucose to repress pGAL-SCC1. Pds1 and Cdc28 were monitored as described for panel A.