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. 2012 Oct 1;2(10):1223–1232. doi: 10.1534/g3.112.003558

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Copyright © 2012 Chang et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution Unported License (http://creativecommons.org/licenses/by/3.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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The esa1 rDNA silencing defect is suppressed by increased gene dosage of NAB3. (A) Diagram and location of rDNA::ADE2-CAN1 silencing marker within the rDNA array on chromosome XII. (B) The esa1 rDNA silencing defect (vector) is restored in cells transformed with an ESA1 plasmid, and by NAB3. Increased dosage of LYS20, LEU2, or VAP1 does not rescue esa1’s rDNA silencing defect. An esa1 strain with the 25S rDNA::ADE2-CAN1 reporter (LPY4911) was transformed with vector (pLP1402), ESA1 (pLP796), LYS20 (pLP1412), NAB3 (pLP1238), VAP1 (pLP1259), SIR2 (pLP37), or LEU2 (pLP1417). To test for rDNA silencing defects, strains were plated on SC-Ade-Arg-Ura (growth) with and without 32 µg/ml canavanine (rDNA silencing) at 33°. (C) NAB3 overexpression (pLP1238) has no effect on rDNA silencing of a WT strain (LPY4909).