Fig. 5: TOP2B colocalizes with endogenous DSB accumulation in thymocytes. | Nature Communications

Fig. 5: TOP2B colocalizes with endogenous DSB accumulation in thymocytes.

From: Endogenous topoisomerase II-mediated DNA breaks drive thymic cancer predisposition linked to ATM deficiency

Fig. 5

a–c Genome browser view of TOP2B, POLR2A, RAD21, and ENDseq (DSBs) signal tracks in wild-type and Atm−/− primary thymocytes, as indicated, at Bcl11b (a), Notch1 (b) and Pten (c) loci. Atm−/−-specific ENDseq peaks, defined as those not called in wild-type thymocytes, are highlighted in yellow. Two regions of interest in Pten are indicated as region 1 and region 2. d Global profile of ENDseq signal at TOP2B peaks in wild-type, Atm−/− and Rag2−/− primary thymocytes. Control input signal is also shown. e Global profile of TOP2B signal at ENDseq peaks in wild-type primary thymocytes. Set of ENDseq peaks were determined as the merge between those detected in any of the analysed genetic conditions.

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