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. 2010 Jul 22;6(7):e1001032. doi: 10.1371/journal.pgen.1001032

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This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration, which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

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(A) Genetic interactions of rqh1Δ mutant with htaAQ, brc1Δ, and brc1-T672A. Five-fold serial dilutions of indicated strains were spotted on YES medium or YES with 2 mM HU and 1 µM CPT. Pictures were taken after 3 days at 30°C. (B) Tetrad dissection of brc1-T672A mutant crossed with rqh1Δ showing two dissected asci. The double mutant (pentagon) has strong synthetic growth defects compared to either parental strain. (C) The loss of Rqh1 function in the htaAQ, brc1Δ, or brc1-T672A mutants leads to cell elongation, chromosome segregations defects and higher levels of aberrant mitosis (indicates by arrows) compared to the individual parental strains. The indicated strains were grown in YES media at 30°C, cells were fixed in cold 70% ethanol, stained with DAPI, and analyzed by fluorescence microscopy. (D) Quantification of (C), error bars represent the range between independent duplicate experiments. (E) γH2A levels increase at the rDNA in the absence of Rqh1. γH2A ChIP was performed in the indicated strains. Primer locations are shown in Figure 5B.