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Over-expression of S. cerevisiae G1 cyclins restores the viability of alg1 N-glycosylation mutants
- Benton, B.K., Plump, S.D., Roos, J., Lennarz, W.J., Cross, F.R.
- Current genetics 1996 v.29 no.2 pp. 106-113
- Saccharomyces cerevisiae, mutants, alleles, proteins, cell division, chemical reactions, glycosyltransferases, structural genes, nucleotide sequences, amino acid sequences, gene expression, messenger RNA, mutation, transcription (genetics)
- In budding yeast, one of three G1 cyclins is required for progression though START, when cells commit to a further round of cell division. We have identified mutations in ALG1 (ERC14), a gene required for N-glycosylation, which are inviable in a cln1 cln2 background but are rescued by over-expression of CLNs. CLN1 and CLN2 are much more efficient than CLN3 in rescuing the erc14-1 allele. The erc14-1 allele results in a significant N-glycosylation defect, and no rescue of this defect by CLN1 over-expression was detected. These data suggest that CLN over-expression could be allowing cells to live with lower levels of N-glycosylation, possibly by overcoming a checkpoint sensitive to N-glycosylation capacity. A plasmid suppressor of alg1, PSA1, encodes a 361 amino-acid protein with homology to NDP-hexose pyrophosphorylases, the enzymes that catalyze the formation of activated sugar nucleotides. PSA1 is an essential gene, and PSA1 transcription is nearly co-ordinately regulated with CLN2 transcription, peaking near START. Co-ordinate regulation of glycosylation, sugar nucleotide metabolism, and cell-cycle progression through G1 may be a feature that ensures adequate cell-wall precursors are present before bud emergence.