SIR protein

Silent Information Regulator (SIR) proteins are involved in regulating gene expression and some SIR family members are conserved from yeast to humans. SIR proteins organize heterochromatin at telomeres,rDNA and at silent loci including, in yeast, the hidden mating type loci. SIR family genes encode 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.

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 George 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 George to consider the hypotheses that the cmt mutants may act by de-repressing silent information.

In the same year that Haber & George 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 and HMα, which would allow an a/a diploid to sporulate and would cause haploid segregants inheriting the mutant allele to behave as a/α diploids despite being haploid. The authors named the mutation MAR for its apparent role in mating type regulation, and were able to map the mutation to chromosome IV, and determined that it was located 27.3 cM from a commonly used trp1 marker.

...
Wikipedia