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. 2021 May 1;35(9-10):698–712. doi: 10.1101/gad.348431.121

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© 2021 Viktorovskaya et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 4. — The pob3-E154K and spt5-QS suppressors do not restore the Spt6-Spn1 interaction. (A) Western blots for Spt6-FLAG co-IP analysis, as in Figure 1A. Spt5 and Spt16 were detected using their respective polyclonal antibodies. (B) Quantification of Spt6-FLAG co-IP experiments (top) and inputs (bottom). Error bars indicate the mean ± standard error of the relative Western blot signal from the replicates shown. The co-IP signal was normalized to the Spt6-FLAG pull-down signal. (C) Assay for the ability of pob3-E154K or spt5-QS to suppress spn1Δ inviability. Growth in the presence of 5-fluoroorotic acid (5-FOA) indicates viability after the loss of a SPN1-URA3 plasmid as the sole source of Spn1. Strains were grown to saturation in YPD, serially diluted 10-fold, and spotted for growth on the indicated media.