Silent Information Regulator (SIR) proteins are involved in regulating gene expression. SIR proteins organize heterochromatin near telomeres, rDNA, and at silent loci including hidden mating type loci in yeast. The SIR family of genes encodes catalytic and non-catalytic proteins that are involved in de-acetylation of histone tails and the subsequent condensation of chromatin around a SIR protein scaffold. Some SIR family members are conserved from yeast to humans. History SIR proteins have been identified in many screens, and have historically been known as SIR (silent information regulator), MAR (mating-type regulator), STE (sterile), CMT (change of mating type) or SSP (sterile suppressor) according to which screen led to their identification. Ultimately, the name SIR had the most staying power, because it most accurately describes the function of the encoded proteins. One of the early yeast screens to identify SIR genes was performed by Anita Hopper and Benjamin Hall, who screened with mutagenesis for alleles that allow sporulation in a normally sporulation-deficient heterothallic α/α (ho/ho MATα/MATα). Their screen identified a mutation in a novel gene that was not linked to HO that allowed the α/α diploid to sporulate, as if it were an α/a diploid, and inferred that the mutation affected a change in mating type by an HO-independent mechanism. Later, it was discovered at the CMT allele identified by Hopper & Hall did not cause a mating type conversion at the MAT locus, but rather allowed the expression of cryptic mating type genes that are silenced in wild-type yeast. In their paper clarifying the mechanism of the CMT mutation, Haber and acknowledge the contribution of Amar Klar, who presented his MAR mutant strains that had similar properties as the CMT mutants at the Cold Spring Harbor Laboratory yeast genetics meeting, which led Haber and to consider the hypothesis that the cmt mutants may act by de-repressing silent information. In the same year that Haber & demonstrated that the cmt mutant restores sporulation by de-repressing hidden mating type loci, two other groups published screens for genes involved in the regulation of silent mating type cassettes. The first study, performed by Amar Klar, Seymour Fogel and Kathy Macleod, identified a mutation in a spontaneous a/a diploid that caused the products of sporulation to be haploids with an apparent diploid phenotype, as assayed by ability to mate. The authors reasoned that the mutation caused the de-repression of then-recently appreciated silent mating type loci HMa