Depletion of the essential poly(A)-binding protein (PAB) in Saccharomyces cerevisiae by promoter inactivation or by the utilization of a temperature-sensitive mutation (pab1-F364L) results in the inhibition of translation initiation and poly(A) tail shortening1. Reversion analysis of pab1-F364L yielded seven independent extragenic cold-sensitive mutations (spbl-spbT) which also suppress a PAB1 deletion. These mutations allow translation initiation without significantly changing poly(A) tail lengths in the absence of PAB, and they affect the amount of 60S ribosomal subunit. Consistent with this, SPB2 encodes the ribosomal protein L46, and its deletion permits the deletion of PAB11 . The SPB4 protein belongs to a family of ATPdependent RNA helicases, and we suspect that the aberrant production of 25S rRNA occurring in spb4-1 mutants also allows the deletion of PAB12. These data suggest that the 60S subunit mediates the PAB requirement of translation initiation, thereby ensuring that only intact poly(A) + mRNA will be translated efficiently in vivo. They also indicate that further characterization of the spb mutations could lend insight into the biogenesis of the ribosome.