BAIT

HNM1

CTR1, L000000433, L000000795, YGL077C
Plasma membrane transporter for choline, ethanolamine, and carnitine; involved in the uptake of nitrogen mustard and the uptake of glycine betaine during hypersaline stress; co-regulated with phospholipid biosynthetic genes and negatively regulated by choline and myo-inositol
Saccharomyces cerevisiae (S288c)
PREY

CHO1

PSS1, CDP-diacylglycerol-serine O-phosphatidyltransferase, L000000327, L000001521, YER026C
Phosphatidylserine synthase; functions in phospholipid biosynthesis; catalyzes the reaction CDP-diaclyglycerol + L-serine = CMP + L-1-phosphatidylserine, transcriptionally repressed by myo-inositol and choline
GO Process (1)
GO Function (1)
GO Component (3)

Gene Ontology Biological Process

Gene Ontology Molecular Function

Gene Ontology Cellular Component

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

Hyper-resistance to nitrogen mustard in Saccharomyces cerevisiae is caused by defective choline transport.

Li ZY, Haase E, Brendel M

The recessive hnm1 mutant allele is responsible for hyper-resistance to nitrogen mustard in Saccharomyces cerevisiae. Transformation with a single-copy HNM1 wild-type allele of such hyper-resistant mutants will restore wild-type sensitivity to nitrogen mustard. By contrast the presence of multi-copy vectors containing HNM1, in either a hyper-resistant hnm1 mutant or an HNM1 wild-type, will lead to a novel, mustard-sensitive phenotype unrelated ... [more]

Curr. Genet. Jun. 01, 1991; 19(6);423-7 [Pubmed: 1878995]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: inviable (APO:0000112)

Curated By

  • BioGRID