Fig. 6
MORC2 dimerization is enhanced in response to DNA damage. a HeLa cells were treated with 8 μM CPT for the indicated times. Lysates were subjected to cross-linking assays, followed by immunoblotting analysis with the indicated antibodies (upper panel). The expression levels of γH2AX in lysates without chemical cross-linking are shown as a control for CPT-induced DNA damage (bottom panel). b HEK293T cells were transfected with HA-MORC2 and HA-MORC2 ∆C82. After 48 h of transfection, total cellular lysates were subjected to cross-linking assay. Immunoblotting analysis was carried out with the indicated antibodies (upper panel). The expression levels of γH2AX in lysates without chemical cross-linking are shown as a control for CPT-induced DNA damage (bottom panel). c HeLa cells were treated with 20 ng/mL EGF for the indicated times and subjected to cross-linking assay (upper panel). The expression levels of phosphorylated EGFR (Y1068) in lysates without chemical cross-linking are shown as a control for the activation of downstream signaling by EGF (bottom panel). d HeLa cells were treated with 200 μM CoCl2 for the indicated times and subjected to cross-linking assay (upper panel). The expression levels of hypoxia-inducible factor 1α (HIF1α) in lysates without chemical cross-linking are shown as a control for the activation of hypoxia signaling by CoCl2 (bottom panel)