Disease relevance of sty1

• Heterothalic phh1 dsiruptant is phenotypically indistinguishable from wis1 deletion mutant, both displaying the same extent of partial sterility and enhanced sensitivity to a variety of stress [1].

High impact information on sty1

• A lethal interaction of spc1 and cdc25 mutations shows that Spc1 promotes the onset of mitosis [2].
• Accordingly, sty1- cells are defective in their response to nutrient limitation, lose viability in stationary phase, and are hypersensitive to osmotic stress, oxidative stress, and UV treatment [3].
• We find that sty2 is allelic to the wis1 MAP kinase kinase and that delta sty1 and delta wis1 cells are unable to grow in high osmolarity medium [4].
• This surprising finding is explained by the observation that ctt1+ basal expression is unaffected in atf1 single mutant and spc1 atf1 double mutant cells, suggesting that unphosphorylated Atf1 represses ctt1+ expression in spc1 cells [5].
• Whereas checkpoint rad mutants fail to arrest division in response to DNA damage, spc1 mutants are defective at resuming cell division after UV exposure [5].

Biological context of sty1

• In addition, sty1(-) cells are sterile and exhibit a G(2) cell cycle delay, indicating additional roles of Sty1 in meiosis and cell cycle progression [6].
• It acts at least in part by activating the MAP kinase homologue sty1; loss-of-function sty1 mutants share many phenotypes with wis1 deletion mutants [7].

Associations of sty1 with chemical compounds

• Expression of the fbp1 gene is negatively regulated by cAMP in response to glucose limitation: induction of fbp1 also requires wis1 and sty1 function [7].
• The pmp3 null mutant, as well as the spc1 and atf1 mutants, is hypersensitive to the cationic antibiotic hygromycin B [8].
• In addition, glyoxalase I activity was increased in stress-activated protein kinase-deficient mutants (wis1 and spc1) [9].

Enzymatic interactions of sty1

• Induction of ste11, a meiosis-specific gene transcription factor, by Stm1 overexpression was enhanced in gpa2-deleted cells but was absent in a deletion mutant of sty1, a key protein kinase that links mitotic control with environmental signals and induces stress-responsive genes [10].

Regulatory relationships of sty1

• Expression of hsp16 in response to nucleotide depletion is regulated via the spc1 MAPK pathway in Schizosaccharomyces pombe [11].

Other interactions of sty1

• Overexpression of mkp1(+), like a sty1 mutation, also causes vegetative cells to elongate [12].
• Expression of the sod1+ gene was induced by oxidative stress and no induction was observed in pap1, prr1 and spc1 mutants [13].

References