Skip to main content
. Author manuscript; available in PMC: 2010 May 1.
Published in final edited form as: DNA Repair (Amst). 2009 Feb 10;8(5):654–663. doi: 10.1016/j.dnarep.2008.12.012

Figure 2. Behavior of Tdp1−/− mice and deficiency in 3′ tyrosyl processing.

Figure 2

(A) Motor activity and latency to fall from the rotarod was determined for male and female mice of each genotype and at each age: 3, 6, and 12 months in top, middle and bottom panels, respectively. Asterisk indicates that at the 3 month assessment, Tdp1−/− female mice were significantly less active than Tdp1+/+ mice, p < 0.05. (B) A radiolabeled (*) 3′-pTyr oligomeric substrate was treated with four-fold serial dilutions of brain tissue homogenates from a Tdp1+/+, Tdp1+/−, or Tdp1−/− mouse for 1 h, subjected to denaturing gel electrophoresis, and phosphorimaged. The percent conversion from the tyrosyl substrate to its phosphate product was calculated by densitometry.