We hypothesize that yeast cells use À1 RF to limit the expression of these proteins in order to maintain the correct stoichiometric balance among telomere associated components. Corollary to this, mutations that alter À1 RF and/or NMD should affect telomere function, and should thus show phenotypic defects similar to those observed in telomerase mutants, e.g. cell cycle progression defects. Indeed, we have isolated numerous such mutants [reviewed in (52) ], and have reported that the mof2-1 and mof5-1 mutants, which affect both NMD and À1 RF tend to accumulate large mother-daughter cells, and/or multiply budded cells, typical of G2/M cell cycle defects (53) . Similarly, upf1D cells have abnormally elongated buds, and decreased telomere lengths (54, 55) . Intriguingly, mof6-1 mutants, which only affect À1 RF, arrest as large, unbudded cells, typical of M-phase exit defects (53) . These observations suggest that stabilization of the mRNAs encoding multiple telomere-associated proteins may have dominant negative effects on telomere homeostasis, and that NMD and À1 RF may regulate different aspects of the cell cycle. Additionally, the central role of Bub3p at the mitotic cell cycle spindle assembly checkpoint and the progeroid phenotypes caused by Bub3p deficiency (56) suggest a more general role for À1 RF in control of cell growth and division. Lastly, the expression of Spr6p during sporulation (57) suggests a role for À1 RF in this developmental process as well. Future studies will dissect the roles of the À1 RF signals in these mRNAs.