Article Abstract:
A biochemical approach was adopted in the study of silencing and used protein affinity chromotography to identify the proteins that interact with the SIR products. The use of a SIR4 affinity column to detect interactions between the SIR4 protein and other proteins in yeast showed that silencing proteins SIR2 and SIR3 and two other proteins of 69 and 110 kDa were tightly bound to an affinity column containing the C-terminal half of SIR4. The 110 kDa protein was identified as UBP3, which is involved in the removal of ubiquitin from proteins. A significant increase in silencing at the telomeres and the HML locus was observed when the UBP3 gene was deleted. This suggests that UBP3 is an inhibitor of silencing. UBP3 is assumed to regulate silencing by controlling the SIR protein complex's activity or assembly.
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Article Abstract:
Detection of the mutations in genes that increase life span by examining the relationship between stress resistance and life span in Saccharomyces cerevisiae indicates that sir 4-42 mutation causes a 30% increase in life span by blocking SIR protein recruitment to telomeres and HM loci, raising their levels in other chromosomal areas. The SIR4 gene contains a silencing component that contributes to the life span increase by Sir4-42. Individual expression of the SIR4 carboxyl terminus affects the silencing at telomeres and HM loci.
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Article Abstract:
Immunostaining of yeast (S. cerevisiae) nuclei was utilized to show re- localization of Sir silencing complex from the telomeres to the nucleolus The relocalization was done through SIR4-42 mutation which involves the removal of Sir4p C terminus redirecting Sir protein complexes to rDNA or AGE locus at which the proteins act to delay aging. UTH4, a new gene which determines the life span in yeast, acts with homologue YGLO23 gene to increase the concentration of silencing proteins at rDNA.
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