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of outstanding interest. The molecular mechanisms of two of the life-extending mutations discovered by an earlier genetic screen, SIR4-42 and UTH4-326, were examined. Using immunofluorescence, SIR4-42 was shown to cause a relocalization of the Sir protein complex from telomeres to the nucleolus, dependent on UTH4 and its homologue YGL023. The same relocalization occurred in old wild-type cells, indicating that the Sir protein complex mitigates an age-related defect in nucleolar function, thereby extending life span.
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