High impact information on CLB1

• Neither CLB1 nor CLB2 is essential; however, disruption of both is lethal and causes a mitotic defect [1].
• Three of these (CLB1, CLB2, and CLB4) encode proteins strongly homologous to G2-specific B-type cyclins [1].
• Levels of SCB1 mRNA and protein were found to be periodic through the cell cycle, with maximum accumulation late, most likely in the G2 interval [2].
• A mutant allele of SCB1 that removes an amino-terminal fragment of the encoded protein thought to be required for efficient degradation during mitosis confers a mitotic arrest phenotype [2].
• Using clb1,2,3,4 cells rescued by conditional overproduction of CLB1, we showed that the CLB genes perform an essential role at the G2/M-phase transition, and also a role in S phase [3].

Biological context of CLB1

• CLB1 and CLB4 seem to be much more important for meiosis than for mitosis and may play some special role in meiosis II [4].
• The arrest phenotype of Mcm1-depleted cells is consistent with low levels of Clb1 and Clb2 kinase [5].
• We show that overexpression of Ndd1 results in the upregulation of both CLB1 and CLB2 transcription, suggesting that the suppression of cdc28-1N by NDD1 may be due to an accumulation of these cyclins [6].
• This delay is eliminated by overproducing Clb1, the major cyclin required for meiosis I [7].
• Ectopic overexpression of Clb1 at early meiotic times advances premeiotic DNA replication, meiotic recombination, and nuclear division, but the coupling between these events is lost [8].

Regulatory relationships of CLB1

• Third, ectopic overexpression of AMA1 is able to stimulate ubiquitination of Clb1p in vitro and degradation of Clb1p in vivo [9].

Other interactions of CLB1

• The previously described CLB1 and CLB2 genes encode a closely related pair of B-type cyclins [10].
• Ndd1 is essential for the expression of CLB1, CLB2, and SWI5, since none of these genes are transcribed in its absence [6].
• The recent finding that individual B-type cyclins (encoded by the genes CLB1-CLB6) can have functions in both processes in the budding yeast Saccharomyces cerevisiae casts doubt on this notion [11].
• In contrast, SBF dissociates from the CLN2 promoter when transcription is repressed during G2 and M phases, suggesting that Clb1-Clb4 repress SBF activity by inhibiting its DNA-binding activity [12].
• Second, Ama1p is required for the degradation of the B-type cyclin Clb1p, an APC/C substrate in both meiotic and mitotic cells [9].

Analytical, diagnostic and therapeutic context of CLB1

• We have cloned four cyclin-B homologs from Saccharomyces cerevisiae, CLB1-CLB4, using the polymerase chain reaction and low stringency hybridization approaches [3].

References