High impact information on MSG5

• Differential input by Ste5 scaffold and Msg5 phosphatase route a MAPK cascade to multiple outcomes [1].
• Genetic analysis indicates that MSG5 acts at a stage where the protein kinases STE7 and FUS3 function to transmit the pheromone-induced signal [2].
• Thus MSG5 might stimulate recovery from pheromone by regulating the phosphorylation state of FUS3 [2].
• Sequence analysis suggests that MSG5 encodes a protein tyrosine phosphatase [2].
• Overexpression of a novel gene called MSG5 suppresses this inhibition of cell division [2].

Biological context of MSG5

• Throughout the range of pheromone concentrations sufficient to cause cell cycle arrest, Gpa1 stimulates adaptive mechanisms that are partially dependent on Msg5 and Mpt5 [3].

Anatomical context of MSG5

• Consistent with a role of this phosphatase on cell wall physiology, cells lacking Msg5 displayed an increased sensitivity to the cell wall-interfering compound Congo Red. We have observed that the N-terminal non-catalytic region of this phosphatase was responsible for binding to the kinase domain of Slt2, the MAPK that operates in this pathway [4].

Physical interactions of MSG5

• Truncation of the Kap104 cargo-binding domain blocked the effect of both Gpa1(E364K) and Msg5 on Fus3-GFP localization [5].

Enzymatic interactions of MSG5

• Reciprocally, Slt2 phosphorylated Msg5 as a consequence of the activation of the cell integrity pathway [4].

Regulatory relationships of MSG5

• POG1 confers alpha-factor resistance when overexpressed and enhances alpha-factor sensitivity when deleted in the background of an msg5 mutant [6].

Other interactions of MSG5

• CLN2 overexpression represses Fus3 kinase activity, independently of the phosphatase Msg5 [7].
• In addition, alternative use of translation initiation sites at MSG5 resulted in two protein forms that are functional on Slt2 and became equally phosphorylated following activation of this MAPK [4].
• We have isolated a novel gene, POG1, whose promotion of recovery parallels that of the MAPK phosphatase Msg5 [6].
• Accumulation of Fus3-GFP in the nuclei of stimulated cells was also inhibited by overexpression of either wild-type Gpa1, the E364K hyperadaptive mutant form of Gpa1, or the Msg5 dually specific phosphatase [5].

References