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. 2018 Aug 29;8(11):3411–3420. doi: 10.1534/g3.118.200589

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Copyright © 2018 Lee et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Suppression of Spt6-Spn1 mutants by set2∆ is epistatic to their enhancement caused by JHD2 overexpression. P_GAL-JHD2 is a construct that replaces the endogenous JHD2 locus. Cells grown in galactose overexpress JHD2 and cells grown without galactose do not express JHD2. (A) Western blot detection of H3K4me3, H3K4me2, H3K4me1, and pan-H3 are shown for extracts prepared from wild- type, P_GAL-JHD2, and P_GAL-JHD2(H427A) cells grown in synthetic complete media containing 2% galactose. Pan-H3 serves as a loading control. (B, C, and D) Plate spot assays (as described in Figure 1) were used to compare the growth of the indicated strains on synthetic media with 2% dextrose (DEX, B) or 2% galactose (GAL, C and D). (E) Genetic interactions of set1∆ and set2∆ with spn1-K192N are shown.