Supplementary Materials for:

ATM directs DNA damage responses and proteostasis via genetically separable pathways

Ji-Hoon Lee, Michael R. Mand, Chung-Hsuan Kao, Yi Zhou, Seung W. Ryu, Alicia L. Richards, Joshua J. Coon, Tanya T. Paull*

*Corresponding author. Email: tpaull{at}utexas.edu

This PDF file includes:

• Fig. S1. Recombinant ATM protein expression.
• Fig. S2. Arsenite and peroxide treatments do not induce DSBs in ATM-inducible U2OS cell lines.
• Fig. S3. The 2RA ATM mutant is deficient in CPT-induced KAP1 phosphorylation.
• Fig. S4. Expression of kinase-deficient ATM sensitizes cells to exogenous stress.
• Fig. S5. U2OS cells expressing wild-type and mutant alleles of ATM have equivalent ratios of cells in S phase.
• Fig. S6. Mitochondrial dysfunction in AT1ABR cells expressing CL ATM.
• Fig. S7. The mKeima mitochondria-targeted pH probe responds to induction or repression of mitophagy.
• Fig. S8. ATM depletion reduces macroautophagy responses of human cells in response to DNA damage or oxidative stress.
• Fig. S9. ATM mutant expression does not alter the predicted phosphorylation targets of CK1 or CDK.
• Fig. S10. CK2 subunit levels are not reduced in A-T cells expressing the CL ATM allele.
• Fig. S11. Expression of CL ATM causes Rad50 accumulation in protein aggregates.
• Legends for tables S1 and S2

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Other Supplementary Material for this manuscript includes the following:

• Table S1 (Microsoft Excel format). Phosphorylated peptides observed in AT1ABR cells with inducibly expressed wild-type, CL, 2RA, or 2RA/CL ATM alleles.
• Table S2 (Microsoft Excel format). Proteins detected in aggregate fractions.
  

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Citation: J.-H. Lee, M. R. Mand, C.-H. Kao, Y. Zhou, S. W. Ryu, A. L. Richards, J. J. Coon, T. T. Paull, ATM directs DNA damage responses and proteostasis via genetically separable pat. Sci. Signal. 11, eaan5598 (2018).

© 2018 American Association for the Advancement of Science