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. 2019 May 1;33(9-10):565–577. doi: 10.1101/gad.320440.118

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© 2019 Leopold et al.; Published by Cold Spring Harbor Laboratory Press

This article, published in Genes & Development, is available under a Creative Commons License (Attribution 4.0 International), as described at http://creativecommons.org/licenses/by/4.0/.

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Figure 1. — The Mit1 N terminus mediates Chp2 interaction and is essential for heterochromatin silencing. (A) Domain diagram of the Mit1 remodeler and the HP1 homologue Chp2. Gray bars correspond to fragments used in B–D and Supplemental Figure S1A,B. (PHD) Plant homeodomain finger; (CD) chromodomain; (CSD) chromoshadow domain; (Clr1ID) Clr1-interacting domain; (N) N terminus; (C) C terminus. (B) Coimmunoprecipitation of endogenously tagged Mit1-13myc and 6xFlag-Chp2. (C) Serial dilution growth assays of wild-type mit1+ and mit1ΔN mutant. Strains were assessed for growth on PMG media, on PMG-ura to monitor otr1R::ura4+ expression, and PMG + FOA to monitor silencing of otr1R::ura4+. Changes in steady-state transcript levels in mutant strains relative to wild-type cells were measured by quantitative real-time RT-qPCR for the otr1::ura4 reporter (C) and for centromeric dg/dh repeats and tlh1 transcripts at telomeres (D). act1 was used as internal standard for all measurements and standard errors were calculated from three independent biological experiments.