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Gene Review

SWI5  -  Swi5p

Saccharomyces cerevisiae S288c

Synonyms: Transcriptional factor SWI5, YD8358.03C, YDR146C
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Disease relevance of SWI5

  • To test this prediction we have expressed the 89-amino-acid sequence of the domain containing the three zinc fingers of SWI5 in Escherichia coli as a cleavable fusion protein, purified under denaturing conditions and folded in vitro [1].

High impact information on SWI5

  • Phosphorylation appears to be the main mechanism controlling the nuclear transport of a number of proteins, including transcription factors such as NFkappaB, c-rel, dorsal, and SWI5 from yeast [2].
  • Swi5p remains at HO for only 5 min [3].
  • As all three serines are phosphorylated by purified CDC28-dependent H1 kinase activity in vitro, we propose a model in which the CDC28 kinase acts directly to control nuclear entry of SWI5 [4].
  • The intracellular localization of the S. cerevisiae transcription factor SWI5 is cell cycle dependent [4].
  • We discovered that SWI5 is found equally concentrated in the nuclei of both mother and daughter cells at the end of anaphase, suggesting that its subsequent fate must somehow differ [5].

Biological context of SWI5

  • SWI5 encodes a zinc-finger protein required for expression of the yeast HO gene [6].
  • Two-hybrid experiments show that amino acids 471 to 513 of Swi5 are necessary and sufficient for interaction with Pho2 and that the SWI5* point mutations cause a severe reduction in this two-hybrid interaction [7].
  • N-terminal amino acid sequence analysis identified the Swi5 stimulatory factor as the product of the GRF10 gene, which encodes a yeast homeodomain protein [6].
  • Swi5 accumulates in the cytoplasm during S, G2, and M phases of the cell cycle but enters the nuclei at late anaphase [8].
  • We have shown that high SIC1 transcript levels at late M phase depend on Swi5 [8].

Anatomical context of SWI5

  • The yeast transcription factors Ace2p and Swi5p regulate the expression of several target genes involved in mating type switching, exit from mitosis and cell wall function [9].
  • This regulation is vital for mother-cell specificity since constitutive transcription of SWI5 causes daughter cells to switch their mating types [10].
  • Ash1p, which only accumulates in daughter cell nuclei, binds to HO soon after Swi5p and aborts recruitment of Swi/Snf, SAGA, and SBF [3].

Associations of SWI5 with chemical compounds

  • In this work we describe an important additional layer of complexity to the current model by identifying a connection between Swi5 and the Mediator/RNA polymerase II holoenzyme complex [11].

Physical interactions of SWI5

  • Grf10 protein purified from a bacterial expression system binds DNA cooperatively with Swi5 in vitro [6].
  • Interactions between Pho85 cyclin-dependent kinase complexes and the Swi5 transcription factor in budding yeast [12].
  • Analysis of CTS1 promoter fragments inserted into a heterologous promoter identify a sequence 90 bp away from the Ace2p binding sites which is required to prevent activation by Swi5p through these binding sites [13].
  • We identified a gene with a Swi5-binding site in the promoter that encoded a protein with high homology to Pcl2, a cyclin-like protein that associates with the Cdk Pho85 [14].
  • The SWI5 gene encodes a zinc finger DNA-binding protein required for the transcriptional activation of the yeast HO gene [15].

Regulatory relationships of SWI5

  • We have shown previously that the Swi5 transcription factor regulates the expression of the SIC1 Cdk inhibitor in late mitosis [14].
  • SIN3 was first identified by a mutation which suppresses the effects of an swi5 mutation on expression of the HO gene in Saccharomyces cerevisiae [16].
  • A version of the HO promoter that has lost its dependence on Start is nevertheless still strongly cell cycle regulated and is activated when SWI5 moves into the nucleus [5].
  • The role of phosphorylation and the CDC28 protein kinase in cell cycle-regulated nuclear import of the S. cerevisiae transcription factor SWI5 [4].
  • EGT2 gene transcription is induced predominantly by Swi5 in early G1 [17].

Other interactions of SWI5

  • Fkh2 protein is associated with the promoters of CLB2, SWI5 and other genes of the cluster [18].
  • Our data suggest that cell cycle-regulated nuclear accumulation of Swi5 is responsible for the burst of SIC1 transcription at the end of anaphase [8].
  • We also found that overexpression of SWI5 caused cell lethality in a pho85 deletion strain [12].
  • This suggests that one function of SIN5 is to prevent ACE2, a SWI5 homolog, from activating HO expression [19].
  • SWI5 encodes a transcription factor paralogous to ACE2 [20].

Analytical, diagnostic and therapeutic context of SWI5

  • We performed both biochemical and genetic tests to discover the biological significance of the interaction between Pcl2 and Swi5 seen in the two-hybrid assay [12].


  1. Zinc-finger motifs expressed in E. coli and folded in vitro direct specific binding to DNA. Nagai, K., Nakaseko, Y., Nasmyth, K., Rhodes, D. Nature (1988) [Pubmed]
  2. Regulation of protein transport to the nucleus: central role of phosphorylation. Jans, D.A., Hübner, S. Physiol. Rev. (1996) [Pubmed]
  3. Ordered recruitment of transcription and chromatin remodeling factors to a cell cycle- and developmentally regulated promoter. Cosma, M.P., Tanaka, T., Nasmyth, K. Cell (1999) [Pubmed]
  4. The role of phosphorylation and the CDC28 protein kinase in cell cycle-regulated nuclear import of the S. cerevisiae transcription factor SWI5. Moll, T., Tebb, G., Surana, U., Robitsch, H., Nasmyth, K. Cell (1991) [Pubmed]
  5. The identification of a second cell cycle control on the HO promoter in yeast: cell cycle regulation of SW15 nuclear entry. Nasmyth, K., Adolf, G., Lydall, D., Seddon, A. Cell (1990) [Pubmed]
  6. The Swi5 zinc-finger and Grf10 homeodomain proteins bind DNA cooperatively at the yeast HO promoter. Brazas, R.M., Stillman, D.J. Proc. Natl. Acad. Sci. U.S.A. (1993) [Pubmed]
  7. Residues in the Swi5 zinc finger protein that mediate cooperative DNA binding with the Pho2 homeodomain protein. Bhoite, L.T., Stillman, D.J. Mol. Cell. Biol. (1998) [Pubmed]
  8. The transcription factor Swi5 regulates expression of the cyclin kinase inhibitor p40SIC1. Knapp, D., Bhoite, L., Stillman, D.J., Nasmyth, K. Mol. Cell. Biol. (1996) [Pubmed]
  9. Overlapping and distinct roles of the duplicated yeast transcription factors Ace2p and Swi5p. Doolin, M.T., Johnson, A.L., Johnston, L.H., Butler, G. Mol. Microbiol. (2001) [Pubmed]
  10. Cell cycle regulation of SW15 is required for mother-cell-specific HO transcription in yeast. Nasmyth, K., Seddon, A., Ammerer, G. Cell (1987) [Pubmed]
  11. The Swi5 activator recruits the Mediator complex to the HO promoter without RNA polymerase II. Bhoite, L.T., Yu, Y., Stillman, D.J. Genes Dev. (2001) [Pubmed]
  12. Interactions between Pho85 cyclin-dependent kinase complexes and the Swi5 transcription factor in budding yeast. Measday, V., McBride, H., Moffat, J., Stillman, D., Andrews, B. Mol. Microbiol. (2000) [Pubmed]
  13. Role of negative regulation in promoter specificity of the homologous transcriptional activators Ace2p and Swi5p. Dohrmann, P.R., Voth, W.P., Stillman, D.J. Mol. Cell. Biol. (1996) [Pubmed]
  14. Swi5 controls a novel wave of cyclin synthesis in late mitosis. Aerne, B.L., Johnson, A.L., Toyn, J.H., Johnston, L.H. Mol. Biol. Cell (1998) [Pubmed]
  15. Long-range interactions at the HO promoter. McBride, H.J., Brazas, R.M., Yu, Y., Nasmyth, K., Stillman, D.J. Mol. Cell. Biol. (1997) [Pubmed]
  16. Genetic interactions between SIN3 mutations and the Saccharomyces cerevisiae transcriptional activators encoded by MCM1, STE12, and SWI1. Wang, H., Reynolds-Hager, L., Stillman, D.J. Mol. Gen. Genet. (1994) [Pubmed]
  17. EGT2 gene transcription is induced predominantly by Swi5 in early G1. Kovacech, B., Nasmyth, K., Schuster, T. Mol. Cell. Biol. (1996) [Pubmed]
  18. Two yeast forkhead genes regulate the cell cycle and pseudohyphal growth. Zhu, G., Spellman, P.T., Volpe, T., Brown, P.O., Botstein, D., Davis, T.N., Futcher, B. Nature (2000) [Pubmed]
  19. Epistasis analysis of suppressor mutations that allow HO expression in the absence of the yeast SW15 transcriptional activator. Stillman, D.J., Dorland, S., Yu, Y. Genetics (1994) [Pubmed]
  20. ACE2, CBK1, and BUD4 in budding and cell separation. Voth, W.P., Olsen, A.E., Sbia, M., Freedman, K.H., Stillman, D.J. Eukaryotic Cell (2005) [Pubmed]
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