Disease relevance of ARR1

• In contrast, a single copy of S. douglasii ARR1 gene is not sufficient to complement the arsenic hypersensitivity of a S. cerevisiae mutant lacking the transcriptional activator Arr1p [1].

High impact information on ARR1

• Like for Yap1p, specific cysteine residues are critical for Yap8p function [2].
• Using chromatin immunoprecipitation assays, we show that Yap8p is associated with the ACR3 promoter in untreated as well as arsenic-exposed cells [2].
• Transcriptional activation of metalloid tolerance genes in Saccharomyces cerevisiae requires the AP-1-like proteins Yap1p and Yap8p [2].
• We show that Yap8p is stabilized in arsenite-exposed cells in a time- and dose-dependent manner [3].
• Collectively, our data is consistent with a model where Yap8p is degraded by the ubiquitin-proteasome pathway in untreated cells, whereas arsenite-exposure results in Yap8p stabilization and gene activation [3].

Biological context of ARR1

• Yap8p forms homodimers in vivo but dimerization is not regulated by arsenite [3].
• In this report, we show that Yap8p is not activated at the transcriptional level but, rather, its nuclear transport is actively regulated and dependent on the exportin chromosome region maintenance protein [4].

Associations of ARR1 with chemical compounds

• Our data also show Yap8-dependent ACR3-lacZ expression was greatly stimulated by arsenite in a dose-dependent manner in the parental strain [5].
• (ii) Acetate-repression might be mediated by the decamer CCCGAG RGGA, present in the promoters of ACS2 and ACR1 [6].

Other interactions of ARR1

• In addition, the transcriptional regulators encoded by YCR020C, YBR083W, and YPR199C were expressed differently in the two strains [7].

References