Functional interaction between the PKC1 pathway and CDC31 network of SPB duplication genes.
Functional interaction between the PKC1 pathway and CDC31 network of SPB duplication genes.
复制标题
PKC1 途径和 SPB 复制基因的 CDC31 网络之间的功能相互作用。
DOI：
10.1093/genetics/155.4.1543
复制
发表时间：
2000
期刊：
影响因子：
3.3
通讯作者：
Rose,MD
中科院分区：
文献类型：
--
作者：
Khalfan,W;Ivanovska,I;Rose,MD
The earliest known step in yeast spindle pole body (SPB) duplication requires Cdc31p and Kar1p, two physically interacting SPB components, and Dsk2p and Rad23p, a pair of ubiquitin-like proteins. Components of thePKC1pathway were found to interact with these SPB duplication genes in two independent genetic screens. Initially,SLG1andPKC1were obtained as high-copy suppressors ofdsk2Δrad23Δ and a mutation inMPK1was synthetically lethal withkar1-Δ17. Subsequently, we demonstrated extensive genetic interactions between thePKC1pathway and the SPB duplication mutants that affect Cdc31p function. The genetic interactions are unlikely to be related to the cell-wall integrity function of thePKC1pathway because the SPB mutants did not exhibit cell-wall defects. Overexpression of multiplePKC1pathway components suppressed the G2/M arrest of the SPB duplication mutants and mutations inMPK1exacerbated the cell cycle arrest ofkar1-Δ17, suggesting a role for thePKC1pathway in SPB duplication. We also found that mutations inSPC110, which encodes a major SPB component, showed genetic interactions with bothCDC31and thePKC1pathway. In support of the model that thePKC1pathway regulates SPB duplication, one of the phosphorylated forms of Spc110p was absent inpkc1andmpk1Δ mutants.
