ArticleCurrent genetics2006
Deletion of RNQ1 gene reveals novel functional relationship between divergently transcribed Bik1p/CLIP-170 and Sfi1p in spindle pole body separation.
Article in Current genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Transcriptomic analysis of Rnq1 loss and prionization reveals alterations in translation pathways and energy metabolism.Scientific reports · 2026Article
- Using High Performance Thin Layer Chromatography-Densitometry to Study the Influence of the Prion [Separations · 2018Article
- Lessons from yeast: the spindle pole body and the centrosome.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014Review
- Extracellular environment modulates the formation and propagation of particular amyloid structures.Molecular microbiology · 2014Article
- Wild yeast harbour a variety of distinct amyloid structures with strong prion-inducing capabilities.Molecular microbiology · 2014Article
- An intrinsically disordered yeast prion arrests the cell cycle by sequestering a spindle pole body component.The Journal of cell biology · 2012Article
- Heterologous prion interactions are altered by mutations in the prion protein Rnq1p.Journal of molecular biology · 2009Article
- An Sfi1p-like centrin-binding protein mediates centrin-based Ca2+ -dependent contractility in Paramecium tetraurelia.Eukaryotic cell · 2007Article
- Defining the limits: Protein aggregation and toxicity in vivo.Critical reviews in biochemistry and molecular biologyReview
- Review
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Authors and funding
2 authors.
Funding
Abstract
Spindle pole body (SPB; the microtubule organizing center in yeast) duplication is essential to form a bipolar spindle. The duplicated SPBs must then separate and migrate to opposite sides of the nucleus. We identified a novel functional relationship in SPB separation between the microtubule stabilizing protein Bik1p/CLIP-170 and the SPB half-bridge protein Sfi1p. A genetic interaction between BIK1 and SFI1 was discovered in a synthetic lethal screen using a strain deficient in the prion protein gene RNQ1. RNQ1 deletion reduced expression from the divergently transcribed BIK1, allowing us to identify genetic interactors with bik1. The sfi1-1 bik1 synthetic lethality was suppressed by over-expression of CIK1, KAR1, and PPH21. Genetic analysis indicated that the sfi1-1 bik1 synthetic lethality was unlikely related to the function of Bik1p in the dynein pathway or to defects in spindle position. Furthermore, a sfi1-1 Deltakip2 mutant was viable, suggesting that the Bik1p pool at the cytoplasmic microtubule plus-ends may not be required in sfi1-1. Microscopic examination indicated the sfi1-1 mutant was delayed in SPB duplication, SPB separation, or spindle elongation and the sfi-1 Deltabik1 double mutant arrested with duplicated but unseparated SPBs. These results suggest that Bik1p has a previously uncharacterized function in the separation of duplicated SPBs.
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