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. 2007 Dec;177(4):2541–2546. doi: 10.1534/genetics.107.079806

Figure 3.—

Figure 3.—

Sir1p and the X element contribute to TPE at VI-R when silencing is compromised. (A) TPE assays. Tenfold serial dilutions were plated to assay silencing. Strains were grown in +Ura −His medium to maintain the S4-CT plasmid. TPE is compromised by the overexpression of the Sir4p C terminus, and this phenotype was exacerbated in the absence of Sir1p or the VI-R X element. (B) Quantitation of TPE. Error bars represent standard deviations. When possible, standard deviations were calculated separately above and below the mean. Values are presented as ratios of TPE level at the wild-type VI-R telomere to TPE level at VI-R in the absence of Sir1p or the X element. When TPE was compromised by S4-CT (striped bars), there was a statistically significant increase in the TPE ratio at VI-R in the absence of Sir1p, in comparison to sir1Δ alone (P < 0.008). When TPE was compromised by SIR4-CT, there was a statistically significant increase in the TPE ratio at VI-R koX, in comparison to the X-element knockout alone (P < 0.04).