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In budding yeast, which possesses simple point centromeres, we discovered that all of its centromeres express long noncoding RNAs (cenRNAs), especially in S phase. Induction of cenRNAs coincides with CENP-A Cse4 loading time and is dependent on DNA replication. Centromeric transcription is repressed by centromere-binding factor Cbf1 and histone H2A variant H2A.Z Htz1 Deletion of CBF1 and H2A.Z   HTZ1  results in an up-regulation of cenRNAs; an increased loss of a minichromosome; elevated aneuploidy; a down-regulation of the protein levels of centromeric proteins CENP-A Cse4 , CENP-A chaperone HJURP Scm3 , CENP-C Mif2 , Survivin Bir1 , and INCENP Sli15 ; and a reduced chromatin localization of CENP-A Cse4 , CENP-C Mif2 , and Aurora B Ipl1 When the RNA interference system was introduced to knock down all cenRNAs from the endogenous chromosomes, but not the cenRNA from the circular minichromosome, an increase in minichromosome loss was still observed, suggesting that cenRNA functions in trans o regulate centromere activity. CenRNA knockdown partially alleviates minichromosome loss in cbf1Δ , htz1Δ , and cbf1Δ htz1Δ in a dose-dependent manner, demonstrating that cenRNA level is tightly regulated to epigenetically control point centromere function.

Point centromere activity requires an optimal level of centromeric noncoding RNA