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

Figure 6.—

Figure 6.—

Suppression of esa1's growth defect by rpd3 is dependent on H4K12. Strains are deleted for all copies of H3 and H4 and carry a TRP1 plasmid with either wild-type H4 or H4 with one mutated lysine residue. Plasmid retention was required for survival. (A) Serial dilutions of the following strains were plated at permissive (30°) and restrictive temperatures (35°) on SC. Top panel: growth of H4K12A mutants in combination with esa1 rpd3. Strains are wild type (LPY12383), H4K12A (LPY12394), esa1 (LPY12384), esa1 H4K12A (LPY12071), esa1 rpd3 (LPY12707), esa1 rpd3 H4K12A (LPY12714), rpd3 (LPY12695), and rpd3 H4K12A (LPY12702). Bottom panel: growth of esa1 rpd3 mutants in combination with each lysine individually mutated to alanine. Strains are esa1 rpd3 (LPY12707), esa1 rpd3 H4K5A (LPY12708), esa1 rpd3 H4K8A (LPY12711), esa1 rpd3 H4K12A (LPY12714), and esa1 rpd3 H4K16A (LPY12717). (B) Suppression of esa1's growth defect through deletion of noncatalytic Rpd3L subunits was also dependent on H4K12. Top panel: twofold dilutions, starting at an A600 of 0.1, were plated on SC−Trp for assaying growth of esa1 sds3 in combination with each lysine individually mutated to alanine. Strains are esa1 sds3 (LPY14175), esa1 sds3 H4K5A (LPY14176), esa1 sds3 H4K8A (LPY14177), esa1 sds3 H4K12A (LPY14178), and esa1 sds3 H4K16A (LPY14179). Bottom panel: as above except in esa1 pho23 mutant. Strains are esa1 pho23 (LPY14165), esa1 pho23 H4K5A (LPY14166), esa1 pho23 H4K8A (LPY14167), esa1 pho23 H4K12A (LPY14168), and esa1 pho23 H4K16A (LPY14169).