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. Author manuscript; available in PMC: 2016 Feb 5.
Published in final edited form as: Mol Cell. 2015 Jan 15;57(3):479–491. doi: 10.1016/j.molcel.2014.12.018

Figure 4. rad50hook mutants are defective in telomere maintenance and Tel1 checkpoint signaling.

Figure 4

A. Telomere lengths of wild-type and rad50hook mutants after 10, 30 and 50 generations of growth at 30°C. Heterozygote diploids (RAD50/ rad50hook) were included as 0 generations of growth. B. Cell survival of rad50hook mutants in a Mec1-deficient background. All strains below the wild-type strain (top row) were mec1Δ sml1Δ. C. Tel1-dependent Rad53 phosphorylation in Mec1-deficient cells upon MMS treatment (+) assessed by western blot. The migration levels of the non-phosphorylated (Rad53) and phosphorylated form (P-Rad53) are indicated. Rad50 genotypes are given above the blot and the Mec1 and Sae2 status (either wild-type or deleted) below.