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. 2018 Sep 8;46(21):11251–11261. doi: 10.1093/nar/gky801

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© The Author(s) 2018. Published by Oxford University Press on behalf of Nucleic Acids Research.

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

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Figure 1. — Genetic interactions between Dot1 overexpression and loss of SAGA-DUB suggest a common function of Dot1 and Ubp8. (A) Strains expressing endogenous Dot1 (WT), no Dot1 (dot1Δ), high levels of Dot1 (P_TDH3-DOT1) or high levels of catalytically inactive Dot1 (P_TDH3-DOT1-G401R) were crossed to an array of ∼1400 mutant strains and examined for fitness. (B) Fitness score (S) of mutants most affected by overexpression of Dot1 where S > 0 represents better growth than expected and S < 0 worse growth than expected. (C) Images of plates as an example of the colony fitness defect of the ubp8Δ strain. (D) Validation of the negative genetic interactions between ubp8Δ and overexpression of Dot1 from a galactose-inducible GAL1 promoter on a multicopy (2 μ) plasmid (+) or using an empty vector control (-).