BAIT

YOP1

YIP2, L000004674, YPR028W
Membrane protein that interacts with Yip1p to mediate membrane traffic; interacts with Sey1p to maintain ER morphology; overexpression leads to cell death and accumulation of internal cell membranes; mutants have reduced phosphatidylserine transfer between the ER and mitochondria; forms ER foci upon DNA replication stress
Saccharomyces cerevisiae (S288c)
PREY

NUP145

RAT10, L000001294, YGL092W
Essential protein with distinct roles in two nuclear pore subcomplexes; catalyzes its own proteolytic cleavage in vivo to generate a C-terminal fragment that is a structural component of the Nup84p subcomplex (with roles in NPC biogenesis and localization of genes to the nuclear periphery), and an N-terminal fragment that is one of several FG-nucleoporins within the NPC central core directly responsible for nucleocytoplasmic transport; homologous to human NUP98
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

ER membrane-bending proteins are necessary for de novo nuclear pore formation.

Dawson TR, Lazarus MD, Hetzer MW, Wente SR

Nucleocytoplasmic transport occurs exclusively through nuclear pore complexes (NPCs) embedded in pores formed by inner and outer nuclear membrane fusion. The mechanism for de novo pore and NPC biogenesis remains unclear. Reticulons (RTNs) and Yop1/DP1 are conserved membrane protein families required to form and maintain the tubular endoplasmic reticulum (ER) and the postmitotic nuclear envelope. In this study, we report ... [more]

J. Cell Biol. Mar. 09, 2009; 184(5);659-75 [Pubmed: 19273614]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: inviable (APO:0000112)

Additional Notes

  • genetic complex
  • nup145{Delta} rtn1{Delta} yop1{Delta} triple mutant

Curated By

  • BioGRID