Integrin β1 activation and enhanced spreading in intoxicated cells is dependent on the DNA damage sensor kinase ATM.

<p><b>A.</b> HeLa cells were left untreated (CTR, dotted line), intoxicated (1μg/ml for 24h, CDT, grey line) or pre-incubated with the ATM inhibitor KU-55933 (5μM, ATMi, black line) prior intoxication. Surface expression of the integrin β1 total levels (left panel) or its activate form (right panel) was assessed by FACS analysis. <b>B.</b> Analysis of cell spreading and formation of focal adhesions was performed in HeLa, CaCo2, and U2OS cells, pre-incubated with the ATM inhibitor as described in A. The panel shows representative micrographs of intoxicated cells left untreated (CDT) or pre-incubated with the ATM inhibitor (CDT-ATMi). The actin cytoskeleton was visualized by phalloidin staining and focal adhesion complexes were visualized using an anti-paxillin antibody. <b>C.</b> Quantification of cell spreading and formation of focal adhesion complexes was performed as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0124119#pone.0124119.g001" target="_blank">Fig 1</a>. The cell area is presented as ratio between the mean of the cell area in intoxicated cells and the mean of the cell area in non-intoxicated cells.