BAIT

VMA2

VAT2, H(+)-transporting V1 sector ATPase subunit B, ATPSV, L000002458, YBR127C
Subunit B of V1 peripheral membrane domain of vacuolar H+-ATPase; an electrogenic proton pump found throughout the endomembrane system; contains nucleotide binding sites; also detected in the cytoplasm; protein abundance increases in response to DNA replication stress
Saccharomyces cerevisiae (S288c)
PREY

PMA1

KTI10, H(+)-exporting P2-type ATPase PMA1, L000001449, YGL008C
Plasma membrane P2-type H+-ATPase; pumps protons out of cell; major regulator of cytoplasmic pH and plasma membrane potential; long-lived protein asymmetrically distributed at plasma membrane between mother cells and buds; accumulates at high levels in mother cells during aging, buds emerge with very low levels of Pma1p, newborn cells have low levels of Pma1p; Hsp30p plays a role in Pma1p regulation; interactions with Std1p appear to propagate [GAR+]
GO Process (4)
GO Function (1)
GO Component (4)

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

Compensatory Internalization of Pma1 in V-ATPase Mutants in Saccharomyces cerevisiae Requires Calcium- and Glucose-Sensitive Phosphatases.

Velivela SD, Kane PM

Loss of V-ATPase activity in organelles, whether through V-ATPase inhibition or V-ATPase (vma) mutations, triggers a compensatory downregulation of the essential plasma membrane proton pump Pma1 in Saccharomyces cerevisiae We have previously determined that the α-arrestin Rim8 and ubiquitin ligase Rsp5 are essential for Pma1 ubiquination and endocytosis in response to loss of V-ATPase activity. Here, we show that Pma1 ... [more]

Genetics Feb. 01, 2018; 208(2);655-672 [Pubmed: 29254995]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: inviable (APO:0000112)

Additional Notes

  • deletion of cnb1 partially inhibits the internalization of PMA1 seen in vma mutants

Curated By

  • BioGRID