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In pre-anaphase cells, Cdc14 is confined to the nucleolus as a subunit of the RENT complex (which also contains Net1/Cfi1 and Sir2), and its phosphatase activity is inhibited by Net1 [ 8 9 10 11 ] . Damaged DNA and mis-oriented mitotic spindles delay exit from mitosis (reviewed in [ 12 ] ), but after errors have been rectified or bypassed, Lte1, Nud1, and possibly other unidentified factors [ 13 ] promote Tem1 activation.
Identified components of the MEN include Tem1 (a GTP-binding protein), Lte1 (a putative guanine nucleotide releasing factor), Nud1 (a spindle-pole-body protein), Cdc15 (a protein kinase), Dbf2/Mob1 (a protein kinase complex), Cdc5 (a Polo-like protein kinase), and Cdc14 (a protein phosphatase).
They encode the GTP-binding protein Tem1 and its putative guanine nucleotide releasing factor Lte1, the dual specificity protein phosphatase Cdc14, protein kinases Cdc5, Cdc15, and Dbf2/Dbf20, the Dbf2-binding protein Mob1 (reviewed in [ 4 ] ) and the spindle-pole-body component Nud1 [ 5 ] . Conditional-lethal temperature sensitive (ts) mutations in any of the MEN genes cause cells to arrest in late mitosis with elevated mitotic Cdk activity when shifted to the restrictive temperature.