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. 2009 Sep;183(1):149–160. doi: 10.1534/genetics.109.103846

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Copyright © 2009 by the Genetics Society of America

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Figure 3.— — Disruption of Rpd3L suppresses esa1 silencing phenotypes. (A) Disruption of Rpd3L suppressed the rDNA silencing defect of an esa1 mutant. Wild type (LPY4909), esa1 (LPY4911), esa1 rpd3 (LPY12147), rpd3 (LPY12145), esa1 sds3 (LPY13517), sds3 (LPY13513), esa1 pho23 (LPY13859), pho23 (LPY13854), esa1 rco1 (LPY13505), and rco1 (LPY13501) all have the rDNA∷ADE2-CAN1 reporter to test for rDNA silencing on plates containing canavanine. Decreased growth on canavanine indicates a defect in rDNA silencing. (B) Disruption of Rpd3L suppressed the telomeric silencing defect of an esa1 mutant. Wild type (LPY4917), esa1 (LPY4919), esa1 rpd3 (LPY12211), rpd3 (LPY12093), esa1 sds3 (LPY13540), sds3 (LPY13536), esa1 pho23 (LPY13769), pho23 (LPY13765), esa1 rco1 (LPY13528), and rco1 (LPY13524) all have the TELVR∷URA3 silencing marker to test for telomeric silencing on plates containing 5-FOA. Decreased growth on 5-FOA indicates a defect in telomeric silencing.