Figure 1. S6K1 protects cells from DNA damaging agents.
(a) Long (S6K1) and short (Iso-2) S6K1 isoform structure and domain organization with addition of Halo-tag (light blue ovals). Isoform Iso-2 lacks 6 out of 12 conserved regions of the kinase domain, a mTOR phosphorylation site at threonine 389 (T389), as well as the C terminal autoinhibitory domain (CTD). NLS (nuclear localization sequence), NTD (N terminal domain). (b) Western blot showing the expression of S6K1 in MEF wild type (WT), S6K-/- cells and S6K-/- cells transduced with retroviruses encoding either empty vector pBABE (pB(-)), S6K1 or Iso-2. (c,f,i) Trypan blue exclusion assay of MEF WT, S6K-/- and S6K-/- cells described in (b) treated with doxorubicin 8 μg/ml (DOX) for 24 hr (c) or 24 hr after either γ irradiation 5 Gy (f) or UVC 8 J/m2/s (i). Data represents means ± SD of six replicates. (d,e,g,h,j) Clonogenic survival assay of MEF WT, S6K-/- cells (d,g,h,j), and S6K-/- cells transduced with retroviruses encoding either empty vector pBABE (pB(-)), S6K1 or Iso-2 (e,g,h,j) treated with various concentrations of Dox (d,e), γ irradiation 1–5 Gy (g), UVC 6.5 J/m2/s (h) or various concentrations of neocarzinostatin (NCS) (j). Colonies were fixed and quantified after 14 days. Data represents means ± SD of at least three biological replicates. (k) Clonogenic survival assay of S6K-/- cells expressing either empty vector pBABE (pB(-))or S6K1. Cells were treated with various concentrations of doxorubicin (DOX) with and without 50 nM rapamycin (R). Data represents means ± SD of three biological triplicates. (l,m) Western blot analysis of MEF WT and S6K-/- cells (l) or cells described in (b) (m) 24 hours after irradiation with UVC 6.5 J/m2/s. Cleaved caspase 3 and γ−H2AX signals were quantified relative to GAPDH signal. * p<0.05, ** p<0.01, *** p<0.001. p values were calculated using Student’s t-test (two-tailed). Data represents means ± SD of three biological triplicates.