FIGURE 7.

OGA inhibition rescued disrupted spindle phenotype in OGT/OGA gain of function cells. GFP, OGT, or OGA gain of function cells were synchronized to M phase and treated with TMG after second thymidine release. a, midzone width and length (mean ± S.E., replicate number (n): nGFP = 198, nOGT = 242, nOGA = 178, nTMG/GFP = 213, nTMG/OGT = 235, nTMG/OGA = 223, *, p < 0.005 GFP versus OGT/OGA, **, p < 0.005 GFP/OGT/OGA versus TMG-GFP/TMG-OGT/TMG-OGA) were quantified using ImageJ software from confocal images stained for DNA and α-tubulin. b, Western blots were probed for O-GlcNAc, OGT, OGA, pT210 PLK1, PLK1, pT323-AurB, AurB, pT288-AurA, AurA, pY15-CDK1, CDK1, GFP, and actin as a load control. c, Western blots were probed for pS10 and total H3. Densitometry of H3 phosphorylation was normalized relative to the level of H3 and averaged from a minimum of three experiments, *, p < 0.005 between GFP versus OGT/OGA.