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Molecular Biology of the Cell logoLink to Molecular Biology of the Cell
. 2006 Jun;17(6):2853.

Correction for “Dsl1p, Tip20p, and the Novel Dsl3(Sec39) Protein Are Required for the Stability of the Q/t-SNARE Complex at the Endoplasmic Reticulum in Yeast”

PMCID: PMC1474785

The authors of “Dsl1p, Tip20p, and the Novel Dsl3(Sec39) Protein Are Required for the Stability of the Q/t-SNARE Complex at the Endoplasmic Reticulum in Yeast” (Mol. Biol. Cell [2005] 16, 3963–3977; published online before print as 10.1091/mbc.E05–01–0056) would like to make the following correction to their paper. The experiment shown in Figure 3B of this paper was erroneously performed with a strain of mating type a rather than α. Thus, the processing observed may have been due to the mating type-specific Bar1 protease. We repeated the experiment using a strain of mating type α at permissive and restrictive temperatures. As shown below (Figure 1), cleavage is observed in dsl3-2 mutants, although to a bit lower extent than in the experiment shown in Figure 3B of our manuscript. Thus, the mating type error did not have a substantive effect on the result and therefore the conclusion remains valid. Nonetheless, to obtain additional independent evidence for a defect in Golgi-ER retrograde transport in dsl3-2 mutants, we performed a mating assay described by Letourneur et al. (1994; Cell 79, 1199–1207). In this assay, mating of mutant cells with a tester strain of opposite mating type depends on the transport of a recombinant pheromone receptor that carries an ER retention signal. Figure 2 shows that diploid cells can form if the mutant cells were exposed to restrictive temperatures for 3 h in the presence of a tester strain. As a positive control, we included strain P82 (sec21-2; Letourneur et al., 1994; Cell 79, 1199–1207). This confirms that Dsl3(Sec39)p is involved in Golgi-ER retrograde transport. Thus, the interpretation of the original experiment was correct, despite the erroneous use of an a, rather than an α, strain.

Figure 1.

Figure 1.

Figure 2.

Figure 2.


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