BAIT

GIC2

L000003314, YDR309C
Redundant rho-like GTPase Cdc42p effector; involved in initiation of budding and cellular polarization; interacts with Cdc42p via the Cdc42/Rac-interactive binding (CRIB) domain and with PI(4,5)P2 via a polybasic region; GIC2 has a paralog, GIC1, that arose from the whole genome duplication
Saccharomyces cerevisiae (S288c)
PREY

BUD2

CLA2, ERC25, L000000199, YKL092C
GTPase activating factor for Rsr1p/Bud1p; plays a role in spindle position checkpoint distinct from its role in bud site selection; required for both axial and bipolar budding patterns; mutants exhibit random budding in all cell types
Saccharomyces cerevisiae (S288c)

Synthetic Lethality

A genetic interaction is inferred when mutations or deletions in separate genes, each of which alone causes a minimal phenotype, result in lethality when combined in the same cell under a given condition.

Publication

The upstream regulator, Rsr1p, and downstream effectors, Gic1p and Gic2p, of the Cdc42p small GTPase coordinately regulate initiation of budding in Saccharomyces cerevisiae.

Kawasaki R, Fujimura-Kamada K, Toi H, Kato H, Tanaka K

BACKGROUND: Cdc42p, a Rho family small GTPase, is essential for budding initiation in the yeast Saccharomyces cerevisiae. The homologous proteins Gic1p and Gic2p (Gic1/2p) are effectors of Cdc42p, but their precise functions remain unknown. Rsr1p/Bud1p is a Ras family small GTPase that controls the selection of the budding site. Previous observations suggested that Rsr1p-GTP recruits Cdc24p, a GDP/GTP exchange factor ... [more]

Genes Cells Mar. 01, 2003; 8(3);235-50 [Pubmed: 12622721]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: inviable (APO:0000112)

Additional Notes

  • GIC1/GIC2/BUD2 triple mutants are synthetic lethal

Curated By

  • BioGRID