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. 2006 Apr 15;20(8):954–965. doi: 10.1101/gad.1409106

Figure 2.

Figure 2.

Nuclear Xrn1 does not rescue the termination defect in rat1-1. (A) NLS-Xrn1 complements the ts growth of rat1-1. The rat1-1 strain (DBY745) was transformed with control vector plasmid (pFL38), WTRat1-GFP (pAJ226), or NLS-Xrn1-GFP (pAJ237) and grown at 25°C or 37°C on SC-Ura plates. As shown previously, NLS-Xrn1 complements growth at 37°C (Johnson 1997). (B) NLS-Xrn1 is recruited to the gene, but it does not complement the termination defect in rat1-1. Anti-pol II (lanes 7–12) and anti-GFP (lanes 13–18) ChIP of galactose-induced GAL1-ADH4 in rat1-1 transformed with vector, RAT1-GFP, or NLS-XRN1-GFP plasmids (DBY768, DBY754, and DBY777). (Lanes 1–6) Titration of input demonstrates linearity of the PCR. HMR is a transcriptionally silent control that was run on a separate gel. Note the failure to terminate at 37°C with NLS-Xrn1 (lane 12) and the cross-linking of NLS-Xrn1 to the ADH4 gene (lanes 17,18). (C) Wild-type and ts mutant Rat1 proteins are recruited to the 3′ end at 25°C and 37°C. ChIP of GFP-tagged Rat1 and Rat1-1 on galactose-induced GAL1-ADH4 in DBY786 (WT) and DBY787 (rat1-1).