Disease relevance of SWI6

• To explore this hypothesis, we expressed Swi4 and Swi6 in insect cells by using the baculovirus system [1].

High impact information on SWI6

• The role of SWI4 and SWI6 in the activity of G1 cyclins in yeast [2].
• SWI4 and SWI6 are transcription factors required for the START-dependent activation of the HO endonuclease gene [2].
• The related Swi4 and Mbp1 proteins are the DNA-binding components of the respective factors, and Swi6 mayhave a regulatory function [3].
• A related factor (MBF) containing SWI6 and a 120K protein binds to the ACGCGTNA (MCB) promoter elements responsible for late G1-specific transcription of DNA replication genes [4].
• A central role for SWI6 in modulating cell cycle Start-specific transcription in yeast [5].

Biological context of SWI6

• Regulation of the yeast DNA replication genes through the Mlu I cell cycle box is dependent on SWI6 [6].
• Surprisingly, a preferential requirement for SWI6 over SWI4 is observed in our studies of ACGCGT-dependent reporter gene expression in vivo [6].
• In this report, the function of SWI6 in meiosis was investigated [7].
• Two of these SWI6 mutants were used in a screen for high copy suppressors of this phenotype [8].
• Although SBF is required for cell viability, SWI6 is not an essential gene [9].

Anatomical context of SWI6

• Taken together, these data indicate that the transcription factor Swi6p and the Rpd3p-based deacetylase complex act in parallel pathways to activate genes required for cell wall biosynthesis [10].

Associations of SWI6 with chemical compounds

• 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 [8].
• We find that swi4, swi6, and hrr25 mutants, but not mbp1 mutants, are sensitive to hydroxyurea and the DNA-damaging agent methyl methane-sulfonate and are defective in the transcriptional induction of a subset of DNA damage-inducible genes [11].
• Both the sensitivity of swi6 mutants to methyl methanesulfonate and hydroxyurea and the transcriptional defect of hrr25 mutants are rescued by overexpression of SWI4, implicating the SBF complex in the Hrr25/Swi6-dependent response to DNA damage [11].
• Alanine substitutions in both TPLH repeats of SWI6 reduce its activity but do not affect the stability of the protein or its association with SWI4 [12].
• Nuclear import of Swi6 occurs concomitantly with dephosphorylation of serine 160 in late M phase [13].

Physical interactions of SWI6

• We show here that SWI4 contains a novel DNA-binding domain at its N terminus that alone binds specifically to SCBs and a C-terminal domain that binds to SWI6 [4].
• G1 transcription factors are differentially regulated in Saccharomyces cerevisiae by the Swi6-binding protein Stb1 [14].

Enzymatic interactions of SWI6

• Furthermore, Cdc28 combined with the S-phase cyclin Clb6 specifically phosphorylates serine 160 of Swi6 in vitro [13].

Regulatory relationships of SWI6

• Furthermore, an increased dosage of SWI6 enhanced the transcript level of the RAD51 gene and also the recombination frequency in meiosis [7].
• The MSN1 and NHP6A genes suppress SWI6 defects in Saccharomyces cerevisiae [8].
• Multiple SWI6-dependent cis-acting elements control SWI4 transcription through the cell cycle [15].
• The G(1) cyclin Cln3 promotes cell cycle entry via the transcription factor Swi6 [16].
• Regulation of SBF by Msn5p is exerted by control of the localization of the regulatory subunit Swi6p [17].

Other interactions of SWI6

• CLN3 function is, however, also dependent on SWI4 and SWI6 [2].
• The HO promoter contains 10 copies of a cell cycle-regulated upstream activation sequence, which is activated by SWI4 and SWI6 [18].
• On the basis of these observations, we suggest that the Rad53-dependent phosphorylation of Swi6 may delay the transition to S phase by inhibiting CLN transcription [19].
• The Swi6 protein interacts with Swi4 to form the SBF complex and with Mbp1 to form the MBF complex [11].
• The transcript levels of the recombination genes RAD51 and RAD54 , which have MCB elements, were reduced in Delta swi6 cells [7].

Analytical, diagnostic and therapeutic context of SWI6

• Site-directed mutagenesis, based on a modeled three-dimensional structure of the swi6p chromodomain, shows that the hydrophobic amino acids which lie in the core of the structure are critical for biological function [20].

References