BAIT

ROT1

L000003404, YMR200W
Molecular chaperone involved in protein folding in ER; mutation causes defects in cell wall synthesis and lysis of autophagic bodies, suppresses tor2 mutations, and is synthetically lethal with kar2-1 and with rot2 mutations; involved in N-linked glycosylation and O-mannosylation; transmembrane helix Ser250 is essential for Rot1p to interact with other membrane components and exert its functional role, avoiding exposure of Ser H-bonding group at lipid-exposed surface
Saccharomyces cerevisiae (S288c)
PREY

SLT2

BYC2, LYT2, MPK1, SLK2, mitogen-activated serine/threonine-protein kinase SLT2, L000001919, YHR030C
Serine/threonine MAP kinase; involved in regulating maintenance of cell wall integrity, cell cycle progression, and nuclear mRNA retention in heat shock; required for mitophagy and pexophagy; affects recruitment of mitochondria to phagophore assembly site (PAS); plays a role in adaptive response of cells to cold; regulated by the PKC1-mediated signaling pathway; SLT2 has a paralog, KDX1, that arose from the whole genome duplication
Saccharomyces cerevisiae (S288c)

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.

Publication

Rot1 plays an antagonistic role to Clb2 in actin cytoskeleton dynamics throughout the cell cycle.

Juanes MA, Queralt E, Bano MC, Igual JC

ROT1 is an essential gene whose inactivation causes defects in cell cycle progression and morphogenesis in budding yeast. Rot1 affects the actin cytoskeleton during the cell cycle at two levels. First, it is required for the maintenance of apical growth during bud growth. Second, Rot1 is necessary to polarize actin cytoskeleton to the neck region at the end of mitosis; ... [more]

J. Cell. Sci. Jul. 15, 2007; 120(0);2390-401 [Pubmed: 17606994]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: vegetative growth (APO:0000106)

Additional Notes

  • deletion causes a growth defect when Rot1 is overexpressed from a doxycycline sensitive promoter

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
SLT2 ROT1
Negative Genetic
Negative Genetic

Mutations/deletions in separate genes, each of which alone causes a minimal phenotype, but when combined in the same cell results in a more severe fitness defect or lethality under a given condition. This term is reserved for high or low throughput studies with scores.

High-0.4271BioGRID
2047210
SLT2 ROT1
Synthetic Lethality
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.

High-BioGRID
484621

Curated By

  • BioGRID