Kc cells treated with CID dsRNA were processed for immunofluorescence to determine whether the localizations of other centromere components were disrupted. a, Control cell showing normal CID and ROD localization. b, Metaphases from RNAi-treated cells. The metaphase on the right shows a small but detectable amount of CID staining, accompanied by a decreased and delocalized amount of ROD staining; the metaphase on the left shows no detectable CID staining and no detectable ROD staining. c, Quantitative immunofluorescence shows that ROD localization depends on the amount of CID present at the kinetochore. d, Metaphase spreads exhibiting varying degrees of CID inhibition. The spread on the left has a small but detectable amount of CID, whereas the spread on the left has no detectable CID. e, Same spreads as in d; the spread with CID has detectable POLO and PROD; the spread on the right has no detectable POLO, but does have detectable, normally localized PROD. f, Quantitative immunofluorescence shows that POLO localization, but not PROD, is dependent on the amount of CID present at the kinetochore. g, h, Mitotic figure lacking detectable CID, also lacks detectable localized BUB1 and MEI-S332. i, Quantitative immunofluorescence shows that both BUB1 and MEI-S332 localization are dependent on the amount of CID present at the kinetochore. j, Mitotic figure with very low CID levels shows no disruption of telomeric or diffuse pericentric HP1 localization. Scale bars, 5 µm (g, h); 10 µm (a, b, d, e, j).