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. 2012 Oct 17;40(22):11435–11449. doi: 10.1093/nar/gks954

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© The Author(s) 2012. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc/3.0/), which permits non-commercial reuse, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com.

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Figure 4. — Defective DNA processing by Mre11-W248R in vivo. (A) Chk1 phosphorylation induced by 90 Gy of IR in Mre11 mutants. Ponceau straining shows loading. (B) Quantitation of ratio of phosphorylated Chk1 over unphophorylated form from representative blot in panel A with basal (-IR) phosphorylation subtracted to specifically reflect IR induced Chk1 activation. Error bars indicate standard deviation from the mean of four independent experiments. (C) Tetrad dissection of spores from cross of rad2Δ (human FEN1 flap endonuclease) to mre11Δ (top right), mre11-W248R (bottom left) and mre11-H134S (bottom right) mutants. Dashed lines indicate predicted genotype. (D) Representative asci from a cross of opposite mating types of indicated mutants. Resulting spore viability is indicated on the bottom right. (E) Mre11-W248R is rescued by deletion of Pku80 in an Exo1 dependent manner. 5-fold serial dilutions of indicated strains were plated and treated with indicated genotoxic agents.