High impact information on SPBC32H8.07

• 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 [1].
• Cells deleted for git11 are defective in glucose repression of both fbp1 transcription and sexual development, resembling cells lacking either the gpa2 Galpha or the git5 Gbeta [1].
• The gpa2 Galpha and git5 Gbeta are both required for glucose-triggered cAMP signaling [1].
• In contrast to another study, we show that git5 is not a negative regulator of the gpa1 Galpha involved in the pheromone response pathway [2].
• The fission yeast git5 gene encodes a Gbeta subunit required for glucose-triggered adenylate cyclase activation [2].

Biological context of SPBC32H8.07

• Disruption of the gpb1 gene indicated that this gene is not required for vegetative cell growth [3].
• Overexpression of the gpb1 gene suppressed this facilitated conjugation and sporulation phenotype of gpb1-disrupted cells but did not cause any obvious effect in wild-type cells [3].
• The git8 gene, identical to gpa2, encodes the alpha subunit of a heterotrimeric guanine-nucleotide binding protein (Galpha) while git5 encodes a Gbeta subunit [4].

Associations of SPBC32H8.07 with chemical compounds

• The git5 Gbeta and git11 Ggamma form an atypical Gbetagamma dimer acting in the fission yeast glucose/cAMP pathway [1].

Regulatory relationships of SPBC32H8.07

• Multicopy gpa2 partially suppresses the loss of git5, while the converse is not true [2].

References