ArticleGenetics1999
The MSN1 and NHP6A genes suppress SWI6 defects in Saccharomyces cerevisiae.
Article in Genetics, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- Repressive chromatin affects factor binding at yeast HO (homothallic switching) promoter.The Journal of biological chemistry · 2011Article
- Identification of novel activation mechanisms for FLO11 regulation in Saccharomyces cerevisiae.Genetics · 2008Article
- Mss11p is a central element of the regulatory network that controls FLO11 expression and invasive growth in Saccharomyces cerevisiae.Genetics · 2005Article
- Multiple pathways for suppression of mutants affecting G1-specific transcription in Saccharomyces cerevisiae.Genetics · 2005Article
- Nhp6 facilitates Aft1 binding and Ssn6 recruitment, both essential for FRE2 transcriptional activation.The EMBO journal · 2004Article
- Spt16-Pob3 and the HMG protein Nhp6 combine to form the nucleosome-binding factor SPN.The EMBO journal · 2001Article
- A bipartite yeast SSRP1 analog comprised of Pob3 and Nhp6 proteins modulates transcription.Molecular and cellular biology · 2001Article
- Chromatin-mediated transcriptional regulation by the yeast architectural factors NHP6A and NHP6B.The EMBO journal · 2000Article
- Architectural transcription factors and the SAGA complex function in parallel pathways to activate transcription.Molecular and cellular biology · 2000Article
- Nhp6: a small but powerful effector of chromatin structure in Saccharomyces cerevisiae.Biochimica et biophysica actaReview
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Ankyrin (ANK) repeats were first found in the Swi6 transcription factor of Saccharomyces cerevisiae and since then were identified in many proteins of eukaryotes and prokaryotes. These repeats are thought to serve as protein association domains. In Swi6, ANK repeats affect DNA binding of both the Swi4/Swi6 and Mbp1/Swi6 complexes. We have previously described generation of random mutations within the ANK repeats of Swi6 that render the protein temperature sensitive in its ability to activate HO transcription. Two of these SWI6 mutants were used in a screen for high copy suppressors of this phenotype. We found that MSN1, which encodes a transcriptional activator, and NHP6A, which encodes an HMG-like protein, are able to suppress defective Swi6 function. Both of these gene products are involved in HO transcription, and Nhp6A may also be involved in CLN1 transcription. Moreover, because overexpression of NHP6A can suppress caffeine sensitivity of one of the SWI6 ANK mutants, swi6-405, other SWI6-dependent genes may also be affected by Nhp6A. We hypothesize that Nhp6A and Msn1 modulate Swi6-dependent gene transcription indirectly, through effects on chromatin structure or other transcription factors, because we have not been able to demonstrate that either Msn1 or Nhp6A interact with the Swi4/Swi6 complex.
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