Disease relevance of MET16

• In the present study, we show that MET16 is the structural gene for PAPS reductase and that the yeast and the Escherichia coli enzymes display significant similarities [1].

High impact information on MET16

• Here, we demonstrate two phases of combinatorial and dynamic H3 methylation during induction of transcription at MET16 in yeast [2].
• Thanks to CY306, we also show that TRXs interact with the phosphoadenosine-5-phosphosulfate (PAPS) reductase MET16 through a conserved cysteine [3].
• A functional comparison of the centromere binding proteins with transcription factors binding at MET16 promoters reveals the strong analogy between centromeres and the MET16 promoter [4].
• MET16-CYC1-lacZ reporter constructs were used to show that MET16 5'-flanking DNA contains a CP1-dependent upstream activation sequence (UAS) [5].
• In most respects, MET16-CYC1-lacZ reporter gene expression mirrored that of chromosomal MET16; however, the endogenous gene was found to be activated in response to amino acid starvation (general control) [5].

Chemical compound and disease context of MET16

• According to our findings, the poplar glutaredoxin can serve as an electron donor to the bacterial 3'-phosphoadenylylsulfate reductase as it supports both the catalysis by the enzyme in vitro and complements a methionine auxotroph strain of Escherichia coli [6].

Biological context of MET16

• We therefore conclude that the GCN4 dependence of MET16 expression is responsible for the decrease in 5' to 3' digestion under stress conditions and that cells use pAp as a signal to limit 5' to 3' RNA degradation under stress conditions [7].
• Two strains with low sulphite production were transformed with high-copy plasmids containing either or both MET14 and MET16 [8].
• Cbf1p is a sequence specific DNA binding protein required for MET16 chromatin remodelling and transcription [9].
• While the deduced amino acid sequence of the sA gene product shows homology with the equivalent MET16 gene product of Saccharomyces cerevisiae, the sC gene product resembles the equivalent MET3 yeast gene product at the N-terminal end, but differs markedly from it at the C-terminal end, showing homology to the APS kinases of several microorganisms [10].
• Irrespective of the level of transcription, repair at the MspI restriction fragment of MET16 exhibits periodicity in line with nucleosome positions in both strands of the regulatory region and the non-transcribed strand of the coding region [11].

Associations of MET16 with chemical compounds

• Gene-enzyme relationship in the sulfate assimilation pathway of Saccharomyces cerevisiae. Study of the 3'-phosphoadenylylsulfate reductase structural gene [1].
• We also analysed the effect of overexpression of MET14 and MET16 on sulphite formation [8].
• The concentration of methionine, adenine, and sulfite in a synthetic grape must influences the progress of fermentation and at the transcriptional level the expression of genes involved in sulfur (MET16), adenine (ADE4), and acetaldehyde (ALD6) metabolism [12].
• Chromatin structure, transcription and repair of cyclobutane pyrimidine dimers at the MET16 gene of wild type, gcn5Delta and ada2Delta Saccharomyces cerevisiae cells were studied under repressing or derepressing conditions [13].
• Because adenosine 3'-5' biphosphate (pAp), which is produced by Met16p, inhibits this degradation pathway to a comparable extent, we were prompted to analyse the role of Met16p in this phenomenon [7].

Other interactions of MET16

• A mutation in the MET4 gene abolishes transcription of both genes MET16 and MET25 [1].
• We employed the MFA2 and MET16 genes as models [9].
• Inhibition of 5' to 3' mRNA degradation under stress conditions in Saccharomyces cerevisiae: from GCN4 to MET16 [7].
• Northern (RNA) blot experiments reveal that the CBF1 protein is required for full induction of MET25 and MET16 gene transcription [14].
• Deletion of GCN5 or ADA2 reduces repair at MET16 [13].

References