High impact information on ccnb1

• The synthesis and destruction of cyclin B drives mitosis in eukaryotic cells [1].
• In cycling extracts from Xenopus embryos, progression into M phase requires the polyadenylation-induced translation of cyclin B1 mRNA [1].
• These observations suggest that regulated cyclin B1 mRNA translation is essential for the embryonic cell cycle [1].
• Cyclin B1 protein and mRNA, whose translation is regulated by polyadenylation, are colocalized with CPEB and maskin [2].
• CPEB interacts with microtubules and is involved in the localization of cyclin B1 mRNA to the mitotic apparatus [2].

Biological context of ccnb1

• The cytoskeleton-dependent localization of cdc2/cyclin B in blastomere cortex during Xenopus embryonic cell cycle [3].
• At the 8th cell cycle, most of the cdc2/cyclin B was localized in the cortical cytoplasm throughout the cell cycle, in the centrosomes and the nucleus at interphase and prometaphase, and in the spindles at metaphase and anaphase [3].
• Here we report that Xenopus cyclin B1 is regulated by both Erk and Plx kinases, and that Cdc2, counter to previous speculation, is not required for CRS phosphorylation [4].
• In contrast, the sudden nuclear accumulation of the complex before entry into mitosis reflects a marked increase in the import rate, with a concomitant inhibition of cyclin B1 nuclear export [4].
• The interphase cytoplasmic location of cyclin B1/Cdc2 reflects continuous, albeit slow, nuclear import and much more rapid nuclear export [4].

Anatomical context of ccnb1

• Cyclin B in Xenopus oocytes: implications for the mechanism of pre-MPF activation [5].
• This kinase activity rises more smoothly than that of the cyclin B-cdc2 complexes and reaches a peak earlier in the cell cycle; indeed, cyclin A is destroyed before nuclear envelope breakdown [6].
• In spite of similar enzymatic properties of cdk5/p26 and p34cdc2/cyclin B kinase, cdk5/p26 did not display M-phase promoting activity when assayed with a cell-free system of Xenopus egg extract [7].
• However, the cyclin A-dependent kinase does not induce a dramatic shortening of centrosome-nucleated microtubules whereas the cyclin B-dependent kinase does, as previously reported [8].
• We have partially characterized this inhibitory pathway as one involving a reversible binding inhibitor of p34cdc2/cyclin B that is tightly associated with cell membranes [9].

Associations of ccnb1 with chemical compounds

• When the blastomeres were treated with nocodazole or latrunculin A at the 8th cell cycle, the amount of cortical cdc2 decreased, but that of cyclin B did not change [3].
• The 26S, but not the 20S proteasome, digested recombinant 49-kD cyclin B at lysine 57 (K57), producing a 42-kD truncated form [10].
• The results of this study indicate that the destruction of cyclin B is initiated by the ATP-dependent and ubiquitin-independent proteolytic activity of 26S proteasome through the first cutting in the NH2 terminus of cyclin (at K57 in the case of goldfish cyclin B) [10].
• However, when all of the Ser phosphorylation sites in the CRS are mutated to Ala to abolish phosphorylation, the mutant cyclin B1Ala is inactivated; activity can be enhanced by mutation of these residues to Glu to mimic phosphoserine, suggesting that phosphorylation of cyclin B1 is required for its biological activity [11].
• Several of the cdc2 mutants were found to affect the kinetics of cyclin B1 and/or mos-induced GVBD upon coinjection, although none affected the rate of progesterone-induced maturation [12].

Physical interactions of ccnb1

• The 42-kD cyclin was also produced by the digestion of native cyclin B forming a complex with cdc2, a catalytic subunit of MPF, and a fragment transiently appeared during cyclin degradation when eggs were released from metaphase II arrest by egg activation [10].

Other interactions of ccnb1

• Prior ablation of Cdc20, addition of methyl-ubiquitin, or addition of nondestructible Delta90 cyclin B rescues the MI-MII transition in Emi1-inhibited oocytes [13].
• However, p34cdc2/cyclin B kinase was distinguished from cdk5/p26 by its binding to p13suc1 protein and by its reactivity to anti-p34cdc2 antibodies [7].
• However, polyadenylation of cyclin B1 and histone B4 mRNA was still observed [14].

Analytical, diagnostic and therapeutic context of ccnb1

• Okadaic acid mimics a nuclear component required for cyclin B-cdc2 kinase microinjection to drive starfish oocytes into M phase [15].
• To investigate the role of cyclin B phosphorylation, we replaced putative cdc2 kinase phosphorylation sites in Xenopus cyclins B1 and B2 by using oligonucleotide site-directed mutagenesis [16].
• Alteration of intracellular compartmentation of metaphase II oocytes either by gentle centrifugation or by cold shock inactivates MAP kinase and targets all cyclin B molecules for full destruction [17].
• Analysis of the parameters of microtubule dynamics by fluorescence video microscopy shows that the dramatic shortening induced by the cyclin B-dependent kinase is correlated with a several fold increase in catastrophe frequency, an effect not observed with the cyclin A-dependent kinase [8].
• The distributions of histone HI kinase activity and of Cdc2 and cyclin B (the catalytic and regulatory subunits of MPF) were followed by dissection of intact eggs following freezing and in cultured fragments separated by ligation [18].

References