Accurate chromosome segregation during cell division is critical to maintain genomic stability. Kinetochore-microtubule bipolar attachment, in which sister chromatids attach to microtubules emanating from opposite spindle poles, ensures chromosome segregation fidelity. Improper kinetochore microtubule attachments activate the spindle assembly checkpoint (SAC) to prevent anaphase onset. Following kinetochore bi-orientation, the SAC is silenced allowing for anaphase onset. The aurora kinase Ipl1, and a centromere-associated protein Sgo1, sense bi-orientation defects and delay anaphase entry. Previous works from our lab and others have found that Ipl1 and Sgo1 in Saccharomyces cerevisiae prevent SAC silencing in the presence of tension defects. How Sgo1 prevents SAC silencing is still unknown. Bub1 kinase facilitates Sgo1-centromere recruitment through phosphorylates H2A and Sgo1 further recruits Rts1. In this study, we find bub1 kinase dead (bub1-KD), phosphodeficient H2A (H2A-121A), and RTS1 deletion mutants all exhibit premature SAC silencing. In the presence of syntelic chromosome attachments, these mutants enter anaphase prematurely and result in high levels of chromosome missegregation. Moreover, these mutants suppress the anaphase entry delay of dam1 phospho-mimicking mutant. Therefore, the centromere recruitment of Sgo1 plays a major role in preventing SAC silencing.