High impact information on TRX1

• Our data further suggest that Skn7 and Yap1 co-operate on the TRX2 promoter, to induce transcription in response to oxidative stress [1].
• TRX2 is already known to be induced by oxidative stress dependent on the Yap1 protein, an AP1-like transcription factor responsible for the induction of gene expression in response to various stresses [1].
• Arabidopsis type h thioredoxin 2 efficiently restored sulfate assimilation whereas Arabidopsis type h thioredoxin 3 conferred H2O2 tolerance [2].
• We expressed eight plant thioredoxins (six cytoplasmic and two chloroplastic) in yeast trx1, trx2 double mutant cells and analyzed the different phenotypes [2].
• To address this discrepancy, we have examined the ability of c-CRD mutant forms of Yap1p to activate expression of an authentic target gene required for H(2)O(2) tolerance, TRX2 [3].

Biological context of TRX1

• The antioxidant activity of thioredoxins is required for both the survival of yeast cells as well as protection against oxidative stress during stationary phase growth, and correlates with an increase in the expression of both TRX1 and TRX2 [4].
• The results suggest that in the absence of TRX1 and TRX2, a slow rate of DNA replication inhibits the normal progress of cellular reproduction [5].
• Deletion of thioredoxin genes TRX1 and TRX2 recapitulated the stimulatory effect of trr1 mutations on MCB reporter gene activity [6].
• From the DNA sequence of the intragenic region TRX1 is 500 bp downstream of PDC1 [7].
• The two genes encoding thioredoxins in Saccharomyces cerevisiae, TRX1 and TRX2, map to chromosome XII and VII, respectively [7].

Associations of TRX1 with chemical compounds

• In addition, the survival rate of the Deltatrx1Delta/trx2 double mutant was approximately 10% of its parent strain when exposed to H(2)O(2.) The MsrA activity was obliterated in Deltatrx1/Deltatrx2 and Deltatrx1 strains and remained intact in the Deltatrx2 and Deltatrx3 strains [8].
• Furthermore, TRX2 gene expression is induced in response to DTT treatment, indicating that thioredoxins form part of the cellular response to a reductive challenge [9].
• However, there does not appear to be a general defect in ER function in thioredoxin mutants, as oxidative protein folding of the model protein carboxypeptidase Y occurs with similar kinetics to the wild-type strain, and trx1 trx2 mutants are unaffected in sensitivity to the glycosylation inhibitor tunicamycin [9].

Other interactions of TRX1

• The Saccharomyces cerevisiae Yap1p transcription factor is required for the H2O2-dependent activation of many antioxidant genes including the TRX2 gene encoding thioredoxin 2 [10].
• Three genes had already been cloned and sequenced: CCT, ADE3 and TR-I [11].

Analytical, diagnostic and therapeutic context of TRX1

• Western blot analysis, using antibody generated against purified 6 x His-tagged Trx1p, showed that both mutant forms of Trx1p were present at the same levels as the wild-type protein [12].
• Electrophoretic mobility shift assays showed that the purified protein can specifically bind the TRX2 target promoter [13].
• Northern blot analysis of stress-induced levels of TRX2 and GSH1 mRNAs indicated that the ability of the mutant Yap1 protein to induce transcriptional activation of target genes correlates well with its ability to confer stress resistance [14].

References