PDF file - 7618K, S1. Analysis of the genetic interaction between 53BP1 and ATM in organismal growth and development. S2. Analysis of ploidy in Trp53bp1-/-/Atm-/- lymphomas. S3. Analysis of Trp53bp1-/-/Atm-/- thymic lymphomas by TCRα/δ locus FISH. S4. SKY analysis of two Trp53bp1-/-/Atm-/- lymphomas. S5. Cell cycle analysis of resting lymphocytes after IR. S6. Aberrant Vd2-Dd1/Dd2-Jd1 coding junctions are not detected in Trp53bp1-/-/Atm-/- mice. S7. Aberrant Vd5-Dd2 Recombination Signal Junctions are not detected in Trp53bp1-/-/Atm-/- mice. S8. Histograms showing the frequency distribution of deletions from each coding end (A-D) and signal end (E-F) analyzed. S9. Cell cycle analysis of activated (cycling) lymphocytes after IR. S10. Analysis of genomic stability in splenic B or T cells treated with olaparib. S11. Analysis of the G2/M checkpoint. α-CD40/IL-4-activated B cells were harvested one hour after exposure to 2 Gy of IR, stained with a FITC-labeled antibody to phospho(P)-histone H3 (Ser10) and propidium iodide (PI) and analyzed by flow cytometry. S12. A second primer set detects deletions at hybrid V(D)J recombination junctions in Trp53bp1-/-/Atm-/- thymic DNA from 7 day-old mice. Table S1. Mendelian ratios in liveborn mice from 53BP1+/-/ATM+/- intercrosses (n=19 litters) Table S2. Analysis of genomic stability in HU-treated B lymphocytes deficient for 53BP1 and/or ATM. Table S3. Analysis of genomic stability in α-CD40+IL-4activated B lymphocytes deficient for 53BP1 and/or ATM. Table S4. Analysis of genomic stability in α-CD40/IL-4 activated B cells deficient for 53BP1 and/or ATM. Metaphase spreads were obtained 24 hr after IR and stained with a telomere probe. Table S5. Analysis of genomic stability in LPS-activated B cells deficient for 53BP1 and/or ATM. Metaphases were obtained 24 hr after exposure to IR and stained with a telomere probe. Table S6. Analysis of genomic stability in T lymphocytes deficient for 53BP1 and/or ATM.