Skip to main content
NCBI home page
The EMBO Journal logoLink to The EMBO Journal
. 1992 Jun;11(6):2087–2093. doi: 10.1002/j.1460-2075.1992.tb05267.x

ARD1 and NAT1 proteins form a complex that has N-terminal acetyltransferase activity.

E C Park 1, J W Szostak 1
PMCID: PMC556675  PMID: 1600941

Abstract

Two yeast genes, ARD1 and NAT1, are required for the expression of an N-terminal protein acetyltransferase. This activity is required for full repression of the silent mating type locus HML, for sporulation, and for entry into G0. While the NAT1 gene product is thought to be the catalytic subunit of the enzyme, the role of the ARD1 protein has remained unclear. We have used epitope tagged derivatives of ARD1 and NAT1 to provide biochemical evidence for the formation of an ARD1-NAT1 complex, and to show that both proteins are required for the N-terminal acetyltransferase activity. We also present evidence for the formation of ARD1-ARD1 homodimers. Deletion analysis suggests that the C-terminal region of ARD1 may be involved in the formation of both ARD1-ARD1 and ARD1-NAT1 complexes.

Full text

PDF
2087

Images in this article

2088Image
on p.2088
2089Image
on p.2089
2090Image
on p.2090
2090Image
on p.2090
2091Image
on p.2091

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Brent R., Ptashne M. A eukaryotic transcriptional activator bearing the DNA specificity of a prokaryotic repressor. Cell. 1985 Dec;43(3 Pt 2):729–736. doi: 10.1016/0092-8674(85)90246-6. [DOI] [PubMed] [Google Scholar]
  2. Bürglin T. R. The yeast regulatory gene PHO2 encodes a homeo box. Cell. 1988 May 6;53(3):339–340. doi: 10.1016/0092-8674(88)90153-5. [DOI] [PubMed] [Google Scholar]
  3. Evan G. I., Lewis G. K., Ramsay G., Bishop J. M. Isolation of monoclonal antibodies specific for human c-myc proto-oncogene product. Mol Cell Biol. 1985 Dec;5(12):3610–3616. doi: 10.1128/mcb.5.12.3610. [DOI] [PMC free article] [PubMed] [Google Scholar]
  4. Field J., Nikawa J., Broek D., MacDonald B., Rodgers L., Wilson I. A., Lerner R. A., Wigler M. Purification of a RAS-responsive adenylyl cyclase complex from Saccharomyces cerevisiae by use of an epitope addition method. Mol Cell Biol. 1988 May;8(5):2159–2165. doi: 10.1128/mcb.8.5.2159. [DOI] [PMC free article] [PubMed] [Google Scholar]
  5. Guarente L., Yocum R. R., Gifford P. A GAL10-CYC1 hybrid yeast promoter identifies the GAL4 regulatory region as an upstream site. Proc Natl Acad Sci U S A. 1982 Dec;79(23):7410–7414. doi: 10.1073/pnas.79.23.7410. [DOI] [PMC free article] [PubMed] [Google Scholar]
  6. Hope I. A., Struhl K. Functional dissection of a eukaryotic transcriptional activator protein, GCN4 of yeast. Cell. 1986 Sep 12;46(6):885–894. doi: 10.1016/0092-8674(86)90070-x. [DOI] [PubMed] [Google Scholar]
  7. Lee F. J., Lin L. W., Smith J. A. N alpha acetylation is required for normal growth and mating of Saccharomyces cerevisiae. J Bacteriol. 1989 Nov;171(11):5795–5802. doi: 10.1128/jb.171.11.5795-5802.1989. [DOI] [PMC free article] [PubMed] [Google Scholar]
  8. Lee F. J., Lin L. W., Smith J. A. N alpha-acetyltransferase deficiency alters protein synthesis in Saccharomyces cerevisiae. FEBS Lett. 1989 Oct 9;256(1-2):139–142. doi: 10.1016/0014-5793(89)81734-x. [DOI] [PubMed] [Google Scholar]
  9. Lee F. J., Lin L. W., Smith J. A. Purification and characterization of an N alpha-acetyltransferase from Saccharomyces cerevisiae. J Biol Chem. 1988 Oct 15;263(29):14948–14955. [PubMed] [Google Scholar]
  10. Ma J., Ptashne M. A new class of yeast transcriptional activators. Cell. 1987 Oct 9;51(1):113–119. doi: 10.1016/0092-8674(87)90015-8. [DOI] [PubMed] [Google Scholar]
  11. Mullen J. R., Kayne P. S., Moerschell R. P., Tsunasawa S., Gribskov M., Colavito-Shepanski M., Grunstein M., Sherman F., Sternglanz R. Identification and characterization of genes and mutants for an N-terminal acetyltransferase from yeast. EMBO J. 1989 Jul;8(7):2067–2075. doi: 10.1002/j.1460-2075.1989.tb03615.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  12. Park E. C., Finley D., Szostak J. W. A strategy for the generation of conditional mutations by protein destabilization. Proc Natl Acad Sci U S A. 1992 Feb 15;89(4):1249–1252. doi: 10.1073/pnas.89.4.1249. [DOI] [PMC free article] [PubMed] [Google Scholar]
  13. Park E. C., Szostak J. W. Point mutations in the yeast histone H4 gene prevent silencing of the silent mating type locus HML. Mol Cell Biol. 1990 Sep;10(9):4932–4934. doi: 10.1128/mcb.10.9.4932. [DOI] [PMC free article] [PubMed] [Google Scholar]
  14. Saiki R. K., Scharf S., Faloona F., Mullis K. B., Horn G. T., Erlich H. A., Arnheim N. Enzymatic amplification of beta-globin genomic sequences and restriction site analysis for diagnosis of sickle cell anemia. Science. 1985 Dec 20;230(4732):1350–1354. doi: 10.1126/science.2999980. [DOI] [PubMed] [Google Scholar]
  15. Whiteway M., Freedman R., Van Arsdell S., Szostak J. W., Thorner J. The yeast ARD1 gene product is required for repression of cryptic mating-type information at the HML locus. Mol Cell Biol. 1987 Oct;7(10):3713–3722. doi: 10.1128/mcb.7.10.3713. [DOI] [PMC free article] [PubMed] [Google Scholar]
  16. Whiteway M., Szostak J. W. The ARD1 gene of yeast functions in the switch between the mitotic cell cycle and alternative developmental pathways. Cell. 1985 Dec;43(2 Pt 1):483–492. doi: 10.1016/0092-8674(85)90178-3. [DOI] [PubMed] [Google Scholar]

Articles from The EMBO Journal are provided here courtesy of Nature Publishing Group

RESOURCES