mik1 and wee1 cooperate in the inhibitory tyrosine phosphorylation of cdc2

Mis3 with a conserved RNA binding motif is essential for ribosome biogenesis and implicated in the start of cell growth and S phase checkpoint

“…The double mutant mis3-224 wee1-50 failed to form colonies in 5 mM HU (data not shown), though single wee1-50 was not HU sensitive. In the absence of HU, the double mutant mis3±224 wee1-50 showed the mitotic catastrophe phenotype at 36 8C (C, upper panel) similar to that found in the other double mutant wee1-50 mik1 null (Lundgren et al 1991) (C, lower panel). The reduced level of Mik1 in mis3-224 mutant as described below may explain this.…”

“…The double mutants between mis3-224 (Takahashi et al e1994) and various mutations noted below were constructed; cdc2-33, cdc6-121, cdc13-117, cdc25-22, cdc10-129 (Nurse et al 1976), cdc2-3w (Enoch et al 1992), Dcyc17/cig2 (Obara-Ishihara & Okayama 1994), Dmik1 (Lundgren et al 1991), wee1-50 (Russell & Nurse 1987), cdc16-116 (Fankhauser et al 1993), cdc17-K42, cdc18-K46 (Nasmyth & Nurse 1981), cdc22-C1 (Fernandez Sarabia et al 1993), swi7-H4 (Singh & Klar 1993), mis5-268, mis11-453 (Takahashi et al 1994, Drad3, Drad9, Drad17, Drad24, Drad25, Dchk1 (Al-Khodairy et al 1994), cut5-T401 (Saka et al 1994), Dcds1 (Murakami & Okayama 1995), Ddis1 (Nabeshima et al 1995), dis3-54 (Kinoshita et al 1991), dis2-11, Ddis2 (Ohkura et al 1989), cut1-21, cut2-364 (Funabiki et al 1996, cut9 (Yamada et al 1997), Dppa1, Dppa2 (Kinoshita et al 1993),Dpck1 (Toda et al 1993), Dtop1, top2-191 (Uemura & Yanagida 1984), and Ddsk1 mutants (Takeuchi & Yanagida 1993). The Mis3-HA integrant was obtained by integrating the HA-tagged mis3 gene at the carboxyl-terminus to replace the genomic mis3 locus.…”

“…Cdc2 kinase plays a key role in ordering the S and M phase (Nurse 1994;MacNeill & Nurse 1997), but little is known of how cells control the onset and duration for the periods of cell mass increase in interphase cell cycle stages. If coordinating control between cell mass and cell cycle is abolished, cells may enter a lethal stage with activation of CDK (cyclin dependent kinase) before reaching normal cell size (Lundgren et al 1991;Enoch et al 1992). It is known that tyrosine phosphorylation at Y15 controls the Cdc2 kinase activity and is important for cell cycle control (Russell & Nurse 1986.…”

Protein kinase D displays intrinsic Tyr autophosphorylation activity: insights into mechanism and regulation

“…For some kinases, however, such a distinction cannot be made so clearly. For example, several predominantly Ser/Thr kinases have been shown to also (auto)phosphorylate Tyr residues 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19. The inverse, a Tyr kinase that also (auto)phosphorylates on Ser/Thr residues, is less common, but occurring nonetheless 20, 21.…”

“…The inverse, a Tyr kinase that also (auto)phosphorylates on Ser/Thr residues, is less common, but occurring nonetheless 20, 21. The role of this ‘dual specificity’ is well‐described for some kinases 9, 10, 18, 19. Other (auto)phosphorylation events are less well understood in terms of function, and sometimes dual specificity is only seen under specific circumstances 19.…”