Disease relevance of STE7

• The presence of the interacting N1-Fus3p adapter increased the infectivity of Ste7p-N2-CT phages approximately 1400-fold, which makes SIP a promising technology for the detection and further investigation of interacting proteins [1].

High impact information on STE7

• Overproduction decreases when haploid ROAM mutants also contain the ste7 mutation which prevents conjugation; other ste mutations do not affect the expression of ROAM mutations [2].
• Kss1 and Fus3, the MAPK targets of Ste7, are required for mating, but their role in invasive growth has been unclear [3].
• We show instead that Kss1 is the principal target of Ste7 in the invasive-growth response in both haploids and diploids [3].
• FUS3/KSS1 phosphorylation depends on two additional kinases, STE11 and STE7 (refs 2, 5, 6) [4].
• Repression of yeast Ste12 transcription factor by direct binding of unphosphorylated Kss1 MAPK and its regulation by the Ste7 MEK [5].

Biological context of STE7

• Order of action of components in the yeast pheromone response pathway revealed with a dominant allele of the STE11 kinase and the multiple phosphorylation of the STE7 kinase [6].
• The signal transduction pathway that mediates the response of haploid yeast cells to peptide mating pheromones involves several components including the protein kinases STE7 and STE11 [6].
• Cell viability was not restored by a mutation in STE7 that blocks signaling downstream of the G protein [7].
• CaSTE7 behaves as a hyperactive allele of STE7, suppressing the mating defects of the pheromone signal-transduction pathway by constitutively stimulating STE12, and hence STE12-dependent processes [8].
• Partial protein sequencing of purified activator indicates that it contains a sequence homologous to kinase subdomains VI and VII of two yeast protein kinases, STE7 and byrl [9].

Anatomical context of STE7

• Sph1p interacts in the two-hybrid system with three mitogen-activated protein (MAP) kinase kinases (MAPKKs): Mkk1p and Mkk2p, which function in the cell wall integrity/cell polarization MAP kinase pathway, and Ste7p, which operates in the pheromone and pseudohyphal signaling response pathways [10].
• We now report that stimulation with serum of COS cells expressing this shares sequence homology with two yeast protein kinases byr1 and STE7 [11].

Associations of STE7 with chemical compounds

• The Ste7 variant has a serine to proline substitution at position 368 [12].
• Ste7 is a serine/threonine/tyrosine kinase of Saccharomyces cerevisiae, which shares 32% identity and 50% similarity with OsSTY kinase in the kinase domains [13].

Physical interactions of STE7

• We also found that both Ste11p and Ste7p interact with Fus3p and Kss1p [14].
• Differences in the ability of constitutive Ste7 variants to bind the MAPKs and Ste5 account for the selective activation of Kss1 [15].

Enzymatic interactions of STE7

• FUS3 and presumably KSS1 are phosphorylated and activated during pheromone induction by a STE7-dependent mechanism [16].

Regulatory relationships of STE7

• MAP kinase-related FUS3 from S. cerevisiae is activated by STE7 in vitro [4].
• Byr1 and Ste7 are in turn regulated by the protein kinases Byr2 and Ste11 [17].
• Upon pheromone stimulation, ubp3 Delta mutants accumulate unconjugated polyubiquitin chains as well as polyubiquitinated forms of the mitogen-activated protein kinase kinase Ste7 [18].

Other interactions of STE7

• In addition, the activity of the MAT alpha 1-LexA fusion protein is dependent on the functions of the STE7, STE11, and STE12 genes that encode components of the pheromone response pathway [19].
• Genetic analysis indicates that MSG5 acts at a stage where the protein kinases STE7 and FUS3 function to transmit the pheromone-induced signal [20].
• Neither protein altered the ability of the mitogen-activated protein kinase (MAPK) Fus3 to feedback phosphorylate a known substrate, the MAPK kinase Ste7 [21].
• Additionally, the cellular projections formed by a pbs2-3 mutant on high osmolarity are absent in strains lacking KSS1 or STE7 [22].
• The ste7, 11, and 12 mutations were not suppressed by ros1 or sst2 [23].

Analytical, diagnostic and therapeutic context of STE7

• We report here the molecular cloning of STE7 and STE11 genes and show that expression of these genes is not regulated transcriptionally by the MAT locus [24].

References