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SPO12 and SIT4 suppress mutations in DBF2, which encodes a cell cycle protein kinase that is periodically expressed
1Laboratory of Yeast Genetics, National Institute for Medical Research, Mill Hill, London, UK.
Abstract:
To help clarify the role of DBF2, a previously described cell cycle protein kinase, high copy number suppressors of the dbf2 mutation were isolated. Three open reading frames (ORF) have been identified. One ORF encodes a protein which has homology to a human small nuclear riboprotein, while the remaining two are genes which have been identified previously, SIT4 and SPO12. SIT4 is known to have a role in the cell cycle but the nature of the interaction between SIT4 and dbf2 is unclear. SPO12 has until now been implicated exclusively in meiosis. However, we show that SPO12 is expressed during vegetative growth, moreover it is expressed under cell cycle control coordinately with DBF2. SPO12 is a nonessential gene, but it becomes essential in a DBF2 delete genetic background. Furthermore, detailed analysis of the cell cycle of SPO12 delete cells revealed a small but significant delay in mitosis. Therefore, SPO12 does have a role during vegetative growth and it probably functions in mitosis in association with DBF2.
Insights
The cell cycle protein kinase DBF2 interacts with SPO12 during vegetative growth. SPO12, previously linked to meiosis, is essential for cell viability when DBF2 is absent and plays a role in mitosis.
Area of Science:
- Molecular Biology
- Cell Biology
- Genetics
Background:
- DBF2 is a known cell cycle protein kinase.
- Understanding DBF2's function requires identifying interacting proteins.
- Previous research linked SPO12 exclusively to meiosis.
Purpose of the Study:
- To elucidate the role of DBF2 in the cell cycle.
- To identify high copy number suppressors of the dbf2 mutation.
- To investigate the function of SPO12 during vegetative growth.
Main Methods:
- Isolation of high copy number suppressors of dbf2 mutation.
- Identification of three open reading frames (ORFs) including SIT4 and SPO12.
- Analysis of SPO12 expression and its role in DBF2 deletion mutants.
Main Results:
- SPO12 is expressed during vegetative growth and is cell cycle-regulated, coordinating with DBF2.
- SPO12 is nonessential but becomes essential in a DBF2 deletion background.
- SPO12 deletion causes a delay in mitosis.
Conclusions:
- SPO12 has a role in vegetative growth and mitosis, likely functioning with DBF2.
- The study reveals a novel function for SPO12 beyond meiosis.
- DBF2 and SPO12 function together in cell cycle regulation.