Expression cloning of a novel suppressor of the Lec15 and Lec35 glycosylation mutations of Chinese hamster ovary cells.

This paper reported the cloning of a cDNA for a new gene, which we termed SL15. We reported that SL15 cDNA corrected two separate glycosylation-defective cell lines known as Lec15 and Lec35. In experiments to be reported in the future we have found that the Lec35 cells used in that study have a defect in the SL15 gene. This provides a clear explanation for correction of Lec35 cells by SL15 cDNA, a result that has now been obtained by three separate individuals in this laboratory as well as by another laboratory (T. Kinoshita, personal communication). However, similar attempts to repeat the correction of Lec15 cells by SL15 cDNA have consistently failed. Based upon further analysis of cell samples from that study, we now conclude that the Lec15 population was contaminated with Lec35 cells. Lec15 cells described in Figs. 2, 3, and 4 as being transfected with SL15 cDNA and having normal glycosylation phenotypes have now been shown to be Lec15-Lec35 hybrids, most likely formed during electroporation. It is likely that SL15 cDNA was carried by contaminating Lec35 cells during expression cloning and that the contaminating Lec35 cells accounted for the greater number of colonies that survived lectin selection after transfection with SL15 cDNA as compared with vector controls.

Since there is no evidence that SL15 cDNA can correct the Lec15 phenotype certain aspects of our paper must be rescinded, specifically Fig. 2, panel C; Fig. 3, all data with T-ptLec15 microsomes; Fig. 4, lane 3; and all sections of the text indicating that SL15 can correct Lec15 cells. However, we remain confident that the correction of Lec35 cells by SL15 cDNA is a valid result. We sincerely apologize to the readers of this journal for any confusion or inconvenience this may have caused.