Before anaphase, kinetochores of sister chromatid (SC) pairs must be attached to microtubules emanating from opposing spindle poles. The conserved Aurora B kinase Ipl1 and its adaptor INCENP/Sli15 correct defective attachments and promote SC bi-orientation. Ame1 and Okp1 are essential components of the COMA sub-complex of the budding yeast central kinetochore, and Ame1 has been demonstrated to physically interact with Sli15. Here, we examine the significance of the Ame1-Sli15 interaction in vivo. We find Sli15 localization at kinetochores is reduced in the absence of Ame1. We demonstrate a role for Ame1 in the correction of defective attachments. While overexpression of OKP1 restores kinetochore localization of the mutant Ame1-4 protein, Sli15 localization is not restored and defective attachments are not corrected. Our findings reveal a new role for the central kinetochore in promoting Sli15 function, and suggest functional Ame1 is required for the correction of defective attachments by promoting the localization of Sli15/INCENP at kinetochores.