As discussed above, we implicate ectopic binding of nuclear CBC to the m7G cap of the U1 snRNP of tgs1∆ cells as a principal factor in the cold sensitivity of tgs1∆ cells. Mutations in the cap-binding site of CBC or deletion of the Snp1 C-terminus completely restore normal growth of tgs1∆ cells at 18°, unlike the dosage suppression by RPO26, which promotes growth of tgs1∆ cells at 18°, albeit not as well as TGS1 or the hypomorphic CBC2 and SNP1-C∆ mutations. These findings fortify the inference that the cold sensitivity of tgs1∆ arises not from the lack of TMG caps, but from the effect of U1-bound CBC on vulnerable yeast mRNAs, among which RPO26 stands out.