Alexias Safi

Alexias is our lab manager. In addition to keeping the lab running smoothly, she is studying how a single amino acid change in Sum1p leads to the ability to spread. In general, repression mechanisms can be categorized as locus-specific or regional. Both types of repression involve alterations in chromatin structure, but locus-specific repressors affect only a few nucleosomes, whereas regional silencing involves specialized chromatin structures that propagate great distances along chromosomes. In budding yeast, the Sum1 complex is a locus-specific repressor. However, the SUM1-1 mutation, which results from the substitution of isoleucine for threonine at position 988, causes the Sum1 complex to associate with different genomic locations and to spread at those new loci. A simple model explaining the change of two properties – genomic location and ability to spread – through a single mutation is that the new genomic locations are more permissive for spreading. However, we tested this model by recruiting wild-type Sum1p to HMR, a location at which mutant Sum1-1p spreads, and found that wild-type Sum1p remained unable to spread (Lynch et al., 2005). Therefore, the ability to spread is a property of the mutant Sum1-1p and not the genomic location. Thus, Sum1-1p presents a useful case-study for exploring the intrinsic properties of chromatin proteins that limit their spreading.

Publication

Safi, A., Wallace, K.A., and Rusche, L.N. (2008) “Evolution of new function through a single amino acid change in the yeast repressor Sum1p.” Mol. Cell. Biol. 28:2567.