Disease relevance of gpa2

• Mutations in gpa2 that are likely to inhibit the GTPase activity of the gene product cause a slight increase in intracellular cAMP levels and result in leaky sterility [1].

High impact information on gpa2

• Cells defective in gpa2 mate and sporulate readily in the presence of plentiful nutrition, bypassing the requirement of nitrogen starvation for the initiation of sexual development [1].
• Disruption of gpa2 slows cell growth but is not lethal [1].
• Cells defective in gpa2 fail to produce cAMP in response to glucose stimulation [1].
• 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 [2].
• Overexpression of the gpa2 Galpha partially suppresses loss of either the git5 Gbeta or the git11 Ggamma, while mutational activation of the Galpha fully suppresses loss of either Gbeta or Ggamma [3].

Biological context of gpa2

• Furthermore, a mutation in either git3 or git5 has an additive effect in strains deleted for gpa2 (git8), as it significantly increases expression of an fbp1-lacZ reporter gene [4].
• Here, we show that gpa2 exhibits a direct and GTP-dependent binding to the Ras-associating domain (RAD) of cyr1, which is identified by a computer algorithm-based search of the cyr1 amino acid sequence [5].
• Fission yeast adenylate cyclase is activated by the gpa2 Galpha subunit of a heterotrimeric guanine-nucleotide binding protein (G protein) [6].

Associations of gpa2 with chemical compounds

• Although both gpa2 (Galpha) and git5 (Gbeta) are required for adenylate cyclase activation, only gpa2 is needed to maintain basal cAMP levels [6].

Regulatory relationships of gpa2

• Mutations in two additional genes, git3 and git5 are suppressed by gpa2+ in high copy number [4].

References