Deletion of RNQ1 gene reveals novel functional relationship between divergently transcribed Bik1p/CLIP-170 and Sfi1p in spindle pole body separation.

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.

journal_name

Curr Genet

journal_title

Current genetics

authors

Strawn LA,True HL

doi

10.1007/s00294-006-0098-6

subject

Has Abstract

pub_date

2006-12-01 00:00:00

pages

347-66

issue

6

eissn

0172-8083

issn

1432-0983

journal_volume

50

pub_type

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