BAIT

LAS17

BEE1, L000003068, L000003581, YOR181W
Actin assembly factor; C-terminal WCA domain activates Arp2/3 complex-mediated nucleation of branched actin filaments and a polyproline domain which can nucleate actin filaments independent of Arp2/3; mutants are defective in actin cytoskeleton dependent processes such as: endocytosis, bud site selection and cytokinesis; localizes with the Arp2/3 complex to actin cortical patches; homolog of the Wiskott-Aldrich Syndrome protein (WASP), implicated in severe immunodeficiency
Saccharomyces cerevisiae (S288c)
PREY

RHO4

Rho family GTPase RHO4, L000001633, YKR055W
Non-essential small GTPase; member of the Rho/Rac subfamily of Ras-like proteins; likely to be involved in the establishment of cell polarity; has long N-terminal extension that plays an important role in Rho4p function and is shared with Rho4 homologs in other yeasts and filamentous fungi
GO Process (3)
GO Function (1)
GO Component (3)
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

Functional interactions between the VRP1-LAS17 and RHO3-RHO4 genes involved in actin cytoskeleton organization in Saccharomyces cerevisiae.

Roumanie O, Peypouquet MF, Thoraval D, Doignon F, Crouzet M

The RGD1 gene from Saccharomyces cerevisiae, which encodes a GTPase-activating protein for the Rho3 and Rho4 small G proteins, exhibits synthetic lethality with the VRP1 and LAS17 genes. Their products are proline-rich proteins that interact with both actin and myosins to ensure polarized growth. By testing functional links, we found that the VRP1 and LAS17 genes are potent suppressors of ... [more]

Curr. Genet. Feb. 01, 2002; 40(5);317-25 [Pubmed: 11935222]

Throughput

  • Low Throughput

Ontology Terms

  • inviable (APO:0000112)

Additional Notes

  • genetic complex
  • overexpression of constitutively active forms of Rho3 and Rho4 inhibit all growth in a Las17 mutant

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
LAS17 RHO4
Synthetic Growth Defect
Synthetic Growth Defect

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

Low-BioGRID
657066

Curated By

  • BioGRID