BAIT

HSP82

HSP90, Hsp90 family chaperone HSP82, L000000822, YPL240C
Hsp90 chaperone; redundant in function with Hsc82p; required for pheromone signaling, negative regulation of Hsf1p; docks with Tom70p for mitochondrial preprotein delivery; promotes telomerase DNA binding, nucleotide addition; protein abundance increases in response to DNA replication stress; contains two acid-rich unstructured regions that promote solubility of chaperone-substrate complexes; HSP82 has a paralog, HSC82, that arose from the whole genome duplication
Saccharomyces cerevisiae (S288c)
PREY

SHE9

MDM33, L000002871, YDR393W
Protein required for normal mitochondrial morphology; mitochondrial inner membrane protein; may be involved in fission of the inner membrane; forms a homo-oligomeric complex
GO Process (2)
GO Function (0)
GO Component (1)

Gene Ontology Biological Process

Gene Ontology Cellular Component

Saccharomyces cerevisiae (S288c)

Phenotypic Enhancement

A genetic interaction is inferred when mutation or overexpression of one gene results in enhancement of any phenotype (other than lethality/growth defect) associated with mutation or over expression of another gene.

Publication

The Phosphorylation Status of Hsp82 Regulates Mitochondrial Homeostasis During Glucose Sensing in Saccharomyces cerevisiae.

Peng G, Hu K, Shang X, Li W, Dou F

Sensing extracellular glucose, budding yeast switches from aerobic glycolysis to oxidative phosphorylation to adapt to environmental changes. During the conversion of metabolic mode, mitochondrial function and morphology change significantly. Mitochondria are the main supply factories of energy for various life activities in cells. However, the research on the signal pathways from glucose sensing to changes in mitochondrial function and morphology ... [more]

J Mol Biol Jul. 01, 2023; 435(13);168106 [Pubmed: 37068581]

Throughput

  • Low Throughput

Ontology Terms

  • phenotype: mitochondrial morphology (APO:0000055)

Additional Notes

  • in the Hsp82S485A strain lacking either FIS1, MDV1, or SHE9, there was a significant increase in cells containing tubular mitochondria

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
HSP82 SHE9
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
166976

Curated By

  • BioGRID