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Gene Review

SPC29  -  Spc29p

Saccharomyces cerevisiae S288c

Synonyms: LPH3, LPH3W, NIP29, Spindle pole component 29, YPL124W
 
 
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High impact information on SPC29

  • We find that Mlp2p binds directly to Spc110p, Spc42p, and Spc29p, which are three core components of the spindle pole body (SPB), the nuclear envelope-associated yeast spindle organizer [1].
  • Here, we describe the identification of BBP1 in a suppressor screen with a conditional lethal allele of SPC29 [2].
  • In addition, we found that Bbp1p interacts with Spc29p and the half-bridge component Kar1p [2].
  • Temperature-sensitive mutants for two of the components, Spc29p and Nud1p, were prepared to partly define their function [3].
  • Spc29p is a component of the Spc110p subcomplex and is essential for spindle pole body duplication [4].
 

Anatomical context of SPC29

 

Other interactions of SPC29

  • In agreement with this, overexpressed Spc29p was found to be a nuclear protein, whereas Spc42p is cytoplasmic [4].

References

  1. The nuclear pore complex-associated protein, Mlp2p, binds to the yeast spindle pole body and promotes its efficient assembly. Niepel, M., Strambio-de-Castillia, C., Fasolo, J., Chait, B.T., Rout, M.P. J. Cell Biol. (2005) [Pubmed]
  2. The Bbp1p-Mps2p complex connects the SPB to the nuclear envelope and is essential for SPB duplication. Schramm, C., Elliott, S., Shevchenko, A., Schiebel, E. EMBO J. (2000) [Pubmed]
  3. Localization of core spindle pole body (SPB) components during SPB duplication in Saccharomyces cerevisiae. Adams, I.R., Kilmartin, J.V. J. Cell Biol. (1999) [Pubmed]
  4. Spc29p is a component of the Spc110p subcomplex and is essential for spindle pole body duplication. Elliott, S., Knop, M., Schlenstedt, G., Schiebel, E. Proc. Natl. Acad. Sci. U.S.A. (1999) [Pubmed]
  5. Analysis of a spindle pole body mutant reveals a defect in biorientation and illuminates spindle forces. Yoder, T.J., McElwain, M.A., Francis, S.E., Bagley, J., Muller, E.G., Pak, B., O'Toole, E.T., Winey, M., Davis, T.N. Mol. Biol. Cell (2005) [Pubmed]
 
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