BAIT

PHO92

YDR374C
Posttranscriptional regulator of phosphate metabolism; facilitates PHO4 mRNA degradation by interacting with Pop2p; regulates PHO4 mRNA stability by binding to PHO4's 3'UTR in a phosphate-dependent manner; contains highly conserved YTH (YT521-B Homology) domain that exhibits RNA-binding activity; functional homolog of human YTHDF2
GO Process (2)
GO Function (1)
GO Component (1)

Gene Ontology Molecular Function

Gene Ontology Cellular Component

Saccharomyces cerevisiae (S288c)
PREY

HAP4

transcription factor HAP4, L000000754, YKL109W
Transcription factor; subunit of the heme-activated, glucose-repressed Hap2p/3p/4p/5p CCAAT-binding complex, a transcriptional activator and global regulator of respiratory gene expression; provides the principal activation function of the complex; involved in diauxic shift
Saccharomyces cerevisiae (S288c)

Affinity Capture-RNA

An interaction is inferred when a bait protein is affinity captured from cell extracts by either polyclonal antibody or epitope tag and associated RNA species identified by Northern blot, RT-PCR, affinity labeling, sequencing, or microarray analysis.

Publication

The S. cerevisiae m6A-reader Pho92 promotes timely meiotic recombination by controlling key methylated transcripts.

Scutenaire J, Plassard D, Matelot M, Villa T, Zumsteg J, Libri D, Seraphin B

N6-Methyladenosine (m6A), one of the most abundant internal modification of eukaryotic mRNAs, participates in the post-transcriptional control of gene expression through recruitment of specific m6A readers. In Saccharomyces cerevisiae, the m6A methyltransferase Ime4 is expressed only during meiosis and its deletion impairs this process. To elucidate how m6A control gene expression, we investigated the function of the budding yeast m6A ... [more]

Nucleic Acids Res Jan. 25, 2023; 51(2);517-535 [Pubmed: 35934316]

Throughput

  • High Throughput

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
PHO92 HAP4
Negative Genetic
Negative Genetic

Mutations/deletions in separate genes, each of which alone causes a minimal phenotype, but when combined in the same cell results in a more severe fitness defect or lethality under a given condition. This term is reserved for high or low throughput studies with scores.

High-0.13BioGRID
2100556

Curated By

  • BioGRID