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Here we ask how Fkh2 represses CLB2. Paper-12479992.
Yeast Hct1 is a regulator of Clb2 cyclin proteolysis. Paper-1169436.
The CLB2 and CLB3 cyclins also accumulate in the cim mutants. Paper-105671.
Failure to interact with Hct1 resulted in stabilization of Clb2. Paper-9067711.
Clb2 co-localizes with the bud site selection protein Bud3. Paper-9984159.
Previous results indicate a connection between Rot1 and the cyclin Clb2. Paper-13322897.
A fraction of Clb2 is degraded during anaphase in the absence of Cdh1. Paper-2149106.
Remarkably, Clb2- Cdc28 activity remains elevated in the overreplicating cells. Paper-536002.
What triggers Pds1p proteolysis and why does it not also trigger that of Clb2p? Paper-1371781.
The Rad50 pathway was more sensitive to the absence of Clb2 than the Rad51 pathway. Paper-10042113.
These effects are abrogated by overexpression of the yeast mitotic cyclins Clb1 and Clb2. Paper-2029367.
The previously described CLB1 and CLB2 genes encode a closely related pair of B-type cyclins. Paper-69294.
Activity assays toward several endogenous substrates, including Clb2 and Pds1, are described. Paper-11090257.
Another closely related forkhead protein, Fkh1p, is also recruited to the CLB2 promoter in vivo. Paper-8543267.
In budding yeast, exit from mitosis is achieved by inactivation of Cdc28/ Clb2 activity. Paper-9183379.
It was previously proposed that Cdh1 is essential for proteolysis of the yeast mitotic cyclin Clb2. Paper-2149106.
Yeast Hct1 recognizes the mitotic cyclin Clb2 and other substrates of the ubiquitin ligase APC. Paper-9067711.
SIC1-0P was lethal when combined with deletion of CLB2, CLB3, or CLB5, the major B-type cyclins. Paper-13345756.
Neither CLB1 nor CLB2 is essential; however, disruption of both is lethal and causes a mitotic defect. Paper-29564.
Cell cycle-regulated transcription of the CLB2 gene is dependent on Mcm1 and a ternary complex factor. Paper-240970.
We have examined the ability of the yeast mitotic cyclin Clb2 to function in cells that lack NAP1. Paper-299608.
About 24% of these proteins were phosphorylated more efficiently by Clb5- Cdk1 than Clb2- Cdk1. Paper-11170084.
Fkh2 protein is associated with the promoters of CLB2, SWI5 and other genes of the cluster. Paper-8402851.
In ubc9 mutants both CLB5, an S-phase cyclin, and CLB2, an M-phase cyclin, are stabilized. Paper-145074.
NAP1 is also required for the ability of Clb2 to induce the switch from polar to isotropic bud growth. Paper-299608.
Control of mitotic events by the Cdc42 GTPase, the Clb2 cyclin and a member of the PAK kinase family. Paper-1637511.
On the other hand, destruction of Clb2p, but not that of Pds1p, depends on the Polo-like kinase, Cdc5p. Paper-1371781.
The essential transcription factor Reb1p interacts with the CLB2 UAS outside of the G2/M control region. Paper-9783876.
Conversely, cdh1Delta mutants were impaired in the degradation of Ase1 and Clb2 but not in that of Pds1. Paper-1195682.
The exit from mitosis is monitored by Cdc14 immunofluorescence and Clb2 Western blots. Paper-10516181.
However, CLB2 overexpression has no suppressive effects on other aspects of the rts1-null phenotype. Paper-1027308.
Active Clb2- Cdc28 kinase complex was purified from yeast cells after inserting the CHH tag into Clb2. Paper-8817921.
Temperature-sensitive ubc9-2 mutants were delayed in proteolysis of Pds1 and of cyclin Clb2 during mitosis. Paper-10332251.
Identification of Clb2 residues required for Swe1 regulation of Clb2- Cdc28 in Saccharomyces cerevisiae. Paper-12836884.
However, DNA replication still cannot occur without the combined action of Cdk1p/Clb5p and Cdk1p/ Clb2p. Paper-9185299.
We demonstrate that the ankyrin repeats of Swi4 mediate the interaction with Clb2/ Cdc28 kinase. Paper-562418.
Mutations in the D box sequences of Clb2 inhibited interaction with Cdc23 both in vivo and in vitro. Paper-9186931.
Gin4 is also required for the ability of Clb2 and Nap1 to promote normal progression through mitosis. Paper-1111925.
They are most related to each other and then to the deduced protein sequence of their adjacent genes CLB1 and CLB2. Paper-106530.
The second wave of Clb2 destruction in telophase requires activation of the Cdc20 homolog, Hct1/ Cdh1. Paper-8468323.
In strains lacking the APC, levels of Clb2 and Clb3 remain constant, but Clb/CDK activity oscillates as cells cycle. Paper-10042116.
This novel Rad50- and Rad51-independent pathway of telomeric recombination also appeared to be controlled by Clb2. Paper-10042113.
The first phase of Clb2 destruction, which lowers the Cdc28- Clb2 kinase activity, is a prerequisite for the second. Paper-8468323.
They also uncover a functional interaction between Cdc28/ Clb2 and MRX during the control of the mitotic cell cycle. Paper-10042113.
Rot1 plays an antagonistic role to Clb2 in actin cytoskeleton dynamics throughout the cell cycle. Paper-13322897.
CLB5 transcript abundance peaks in G1, coincident with the CLN2 transcript but earlier than the CLB2 transcript. Paper-69295.
In G2 and M phases, the transcriptional activity of SCB-binding factor is repressed by the mitotic Clb2/ Cdc28 kinase. Paper-562418.
In this pathway, Clb2 initiates a series of events that lead to the mitosis-specific activation of the Gin4 protein kinase. Paper-1637511.
We show that the mitotic CDK Clb2/ Cdc28 functions upstream of Cdc42 in regulating filamentous differentiation. Paper-10983477.
Thus, Clb5 and Clb2 use distinct mechanisms to enhance the phosphorylation of S-phase and M-phase substrates. Paper-11170084.
Ndd1 is essential for the expression of CLB1, CLB2, and SWI5, since none of these genes are transcribed in its absence. Paper-1829609.
In Saccharomyces cerevisiae, Fkh2 both activates and represses transcription of CLB2, encoding a B-type cyclin. Paper-12479992.
Clb2/ Cdc28 kinase is not required for the repression of MCB-binding factor transcriptional activity in G2 and M phase. Paper-562418.
This study shows that the expression of Clb2 during S phase in cells lacking Clb5 failed to rescue late origin activation. Paper-8556620.
Cdh1 and Sic1 may be required for further inactivation of Clb2- Cdk1, regulating cell size and the length of G1. Paper-9183251.
However, disrupting CDC55, a PP2A regulatory subunit, suppressed the Cdc6p-dependent delay of Pds1 and Clb2 destruction. Paper-12430446.
Furthermore, SW14 associates with CLB2 protein and is a substrate for the CLB2- associated CDC28 kinase in vitro. Paper-101863.
We replaced the early-expressed CLB5 coding sequence with the late- expressed CLB2 coding sequence, at the CLB5 locus. Paper-1951184.
However, how Clb2 and the partially redundant cyclin Clb1 confer specificity to Cdk1 in these processes still remains unclear. Paper-13102695.
Ubiquitination and subsequent proteolysis of the mitotic regulators Clb2 and Pds1 depend on the cyclosome/APC and the 26S proteasome. Paper-1850520.
Indeed, early expressed Clb2- Cdk1 can activate all essential Clb-Cdk substrates in a strain lacking all other Clbs and Swe1. Paper-11126644.
Deltaclb1,3,4 Deltabud3 cells, which fail to localize Clb2 to the bud neck, also exhibit a Swe1-dependent elongated bud phenotype. Paper-12372762.
One was the ANP1 gene, which encodes a glycosyltransferase previously identified by a similar strategy using Clb2 instead of Clb3. Paper-8667089.
Blocking APCCdh1-mediated Clb2 proteolysis and chromosome re-duplication does not require Mad2 but a different protein, Bub2. Paper-1888209.
Genetic experiments revealed that loss of either Clb5p or Clb2p cyclins suppresses the mcm5- bob1 mutation and prevents bypass. Paper-9185299.
Cdc20 is essential for the cyclosome- mediated proteolysis of both Pds1 and Clb2 during M phase in budding yeast. Paper-1401489.
In acm1Delta strains, Cdh1 localization to the bud neck and association with two substrates, Clb2 and Hsl1, were strongly enhanced. Paper-12338537.
However, the addition of Acm1 decreases Clb2 ubiquitination when using either phosphorylated or nonphosphorylated Cdh1. Paper-13115081.
The cyclin-dependent kinase Cdc28p associates with the cyclin Clb2p to induce mitosis in the yeast Saccharomyces cerevisiae. Paper-8733593.
Here, we show that Ats1p interacts with Nap1p, a cytoplasmic protein that regulates the activity of the Cdc28p/ Clb2p complex. Paper-10172320.
Moreover, after a shift to the non-permissive temperature, the pph21-102 cells were blocked in G2 and had low activity of Clb2- Cdc28 kinase. Paper-275324.
This result points to possible existence of a Cdc42-MAPK- Clb2/ Cdc28 positive feedback loop in the signalling of filamentous differentiation. Paper-10983477.
Thus, Swe1 regulation and expression timing are key mechanisms that sequester the broad activity of Clb2- Cdk1 from critical substrates. Paper-11126644.
Strikingly, our in vivo data indicate that Swe1 inhibits the kinase activity of Clb2- Cdk1, but not that of Clb5- Cdk1. Paper-12021172.
This arrest results from the regulation of the M-phase cyclin Clb2p at the transcriptional level through the transcription factor Fkh2p. Paper-10652143.
Like a clb2 Delta mutation, each confers tubular bud shape, apically polarized actin distribution, unipolar budding, and delayed anaphase. Paper-8875708.
Sin3 and its catalytic subunit Rpd3 associate with the CLB2 promoter during the G1 phase of the cell cycle. Paper-12544014.
The present data reveal an unexpected role of Cdc28/ Clb2 in telomeric recombination during telomerase-independent maintenance of telomeres. Paper-10042113.
Finally, we show that phosphorylation of T319 and recruitment of Ndd1p to CLB2 and SWI5 promoters is dependent on Cdc28-Clb kinase activity. Paper-9768246.
However, a second fraction of Clb2 remains stable during anaphase and is degraded in a Cdh1-dependent manner as cells exit from mitosis. Paper-2149106.
All lethal combinations included the clb2 deletion, whereas the clb1 clb3 clb4 triple mutant was viable, suggesting a key role for CLB2. Paper-69294.
To analyze the role of Cdc15 during sporulation, a conditional mutant in which CDC15 expression was controlled by the CLB2 promoter was used. Paper-12503765.
The assembly of the ternary complex inhibits ubiquitination of Clb2 in vitro by blocking the interaction of Cdh1 with Clb2. Paper-13115081.
Importantly, deletion of CLB2, a gene encoding a mitotic cyclin, suppresses the temperature-sensitive growth phenotype of prg1 mutant strains. Paper-115654.
Here we show that during mitosis, both the inactivation of Cdc28- Clb2 kinase and the degradation of mitotic cyclin Clb2 occur in two steps. Paper-8468323.
The first phase of Clb2 proteolysis, which commences at the metaphase-to-anaphase transition when Clb2 abundance is high, is dependent on Cdc20. Paper-8468323.
In wild-type cells the CLB5 protein is unstable throughout the cell cycle, whereas CLB2 turnover occurs only at a specific cell-cycle stage. Paper-145074.
Cytoplasmic Clb2 is required for timely inactivation of the mitotic inhibitor Swe1 and normal bud morphogenesis in Saccharomyces cerevisiae. Paper-12372762.
This phosphorylation event is required for the normal temporal expression of cell-cycle-regulated genes such as CLB2 and SWI5 in G2/ M phases. Paper-12329497.
Overproduction of Ndd1 also enhances the expression of SWI5, whose transcription, like that of CLB1 and CLB2, is activated in the late S phase. Paper-1829609.
Another gene, CLB3, was cloned using PCR, CLB1 and CLB2 encode a pair of closely related proteins; CLB3 and CLB4 encode a second pair. Paper-29564.
Early expression of Clb2 in cells lacking both Clb5 and Clb6 did not activate early origins on schedule to restore the correct S phase entry time. Paper-8556620.
The Isw2 chromatin-remodeling ATPase cooperates with the Fkh2 transcription factor to repress transcription of the B-type cyclin gene CLB2. Paper-12479992.
Instead, overexpression of NDD1 prevents the formation of one of the complexes whose appearance correlates with the termination of CLB2 expression in G1. Paper-1829609.
These phosphorylation-dependent changes in the Fkh2p-Ndd1p complex play an important role in the cell cycle- regulated expression of the CLB2 cluster. Paper-10604593.
Interestingly, the B-type cyclin Clb2 is partially stable during premature activation of mitotic exit in a cdc55 mutant, indicating mitotic exit is incomplete. Paper-10812794.
Pds1p proteolysis depends on a WD-repeat protein called Cdc20p, whereas Clb2p proteolysis depends on another, related WD protein called Hct1/Cdh1p. Paper-1371781.
Clb1 and Clb2, whose pattern of expression is similar to that of other known Clbs, are likely to have a role predominantly in the regulation of M phase. Paper-85772.
Cdc28 activation is inhibited by phosphorylation of Cdc28 on tyrosine 19, and by delayed accumulation of the B-type cyclins Clb1 and Clb2. Paper-214007.
Mutations in the NES of Cdc14p allow Clb2p degradation and mitotic exit, but cause abnormal morphology and cytokinesis defects at non-permissive temperatures. Paper-11534399.
The Dbf2 protein kinase functions as part of the mitotic-exit network (MEN), which controls the inactivation of the Cdc28- Clb2 kinase in late mitosis [1]. Paper-8967756.
The Isw2 chromatin-remodeling ATPase cooperates with Fkh2 to remodel the chromatin and repress CLB2 expression throughout the cell cycle. Paper-12479992.
Mutation of the Cdc20 phosphorylation sites permitted the interaction of Cdc20 with Clb2 under conditions that should halt cell cycle progression. Paper-10204591.
Our results demonstrate that the endoribonuclease RNase MRP specifically cleaves the CLB2 mRNA in its 5'-UTR to allow rapid 5' to 3' degradation by the Xrn1 nuclease. Paper-10212324.
These data indicate that Clb2p exists in multiple places in the yeast cell, possibly allowing Cdc28p to locally phosphorylate substrates at distinct subcellular sites. Paper-8733593.
The putative targets include the messages for MID2, MTL1, WSC2, SRL1, EGT2, CLB2, ASH1, and Khd1p colocalizes with these mRNAs at the bud-tip. Paper-13060391.
Fkh2 recruits the coactivator Ndd1, an interaction which is promoted by Clb2/Cdk1-dependent phosphorylation of Ndd1, suggesting that CLB2 is autoregulated. Paper-12479992.
Several genetic interactions suggest a link between Rot1 and the ubiquitin-proteasome system and we show that the Clb2 cyclin is not properly degraded in rot1 cells. Paper-13322897.
By coimmunoprecipitation, we show that Swi4 but not Mbp1 interacts with Clb2/ Cdc28 kinase in vivo during the G2 and M phases of the cell cycle. Paper-562418.
The marked periodicities of CLN2 and CLB2 (mitotic cyclin) transcription were readily evident from cellular yEGFP3-Cln2(PEST) levels with this non-perturbing approach. Paper-8594903.
We show that both FKH1 and FKH2 play essential roles in the activation of the CLB2 cluster genes during G2-M and in establishing their transcriptional periodicity. Paper-8543267.
One of the S. cerevisiae homologues, ALK1, is a member of the CLB2 gene cluster that peaks in expression at M phase and thus may function in mitosis. Paper-9673977.
On the other hand, Clb1 and Clb2 were expressed and activated p34cdc28 later in the mitotic cell cycle, starting in late S phase and continuing up to mitosis. Paper-85772.
Overexpression of Cln2p, but not Clb2p or Clb5p, causes a quantitative shift of Ste20p to the reduced mobility form, and this shift is dependent on Cdc28p activity. Paper-1610584.
We show that Fkh2 controls a repressive chromatin structure that initiates in the early coding region of CLB2 and spreads up the promoter during the M and G(1) phases. Paper-12479992.
Therefore, S-phase accumulated Swe1 prevents Clb2- Cdk1-mediated mitotic activities, but has little effects on Clb5- Cdk1-associated S-phase progression. Paper-12021172.
This signaling network appears to require the function of a Clb2- binding protein called Nap1, the Cdc42 GTPase, and two protein kinases called Gin4 and Cla4. Paper-2050477.
To test whether these genes are required for cyclin ubiquitination, we prepared extracts from G1-arrested yeast cells capable of conjugating ubiquitin to the B-type cyclin Clb2. Paper-890642.
These cells had higher total amounts of Clb2- Cdc28 kinase activity, but the Clb2-normalized specific activity was lower in the pph21-102 cells compared with wild-type cells. Paper-275324.
In yeast, anaphase entry depends on Pds1 proteolysis, while chromosome re-duplication in the subsequent S-phase involves degradation of mitotic cyclins such as Clb2. Paper-1888209.
In addition, the related factors Isw1 and Fkh1 configure the chromatin at the early coding region and negatively regulate CLB2 expression but only during G(2)/M phase. Paper-12479992.
In hct1 mutants, the mitotic cyclin Clb2 is highly stabilized and inappropriately induces DNA replication, while G1 cyclins and other proteolytic substrates remain short-lived. Paper-1169436.
Mutations in different cyclin genes ( CLN3, CLB5, and CLB2) and two cell cycle transcriptional regulators ( SWI4 and MBP1) also suppress the silencing defect at HMR. Paper-268104.
Dynein asymmetry depended on the bud neck kinases Elm1, Hsl1, and Gin4, on the spindle pole components Cnm67 and Cdk1, and on the B-type cyclins Clb1 and Clb2. Paper-11308247.
Our results demonstrate that Clb2 is unable to carry out its full range of functions without NAP1, even though Clb2/p34CDC28-associated kinase activity rises to normal levels. Paper-299608.
The buildup of Clb2 protein is not the result of a defect in the release of the Cdc14 phosphatase from the nucleolus, but rather the result of an increase in CLB2 mRNA levels. Paper-9322189.
In telomerase-positive cells, a synthetic growth defect between mutations in CLB2 and RAD50 or in its partners in the conserved MRX complex, MRE11 and XRS2, was observed. Paper-10042113.
In budding yeast, a protein kinase called Gin4 is specifically activated during mitosis and functions in a pathway initiated by the Clb2 cyclin to control bud growth. Paper-1643178.
This inhibition requires that Clb2 be induced before Cdc6, an initiation protein required for pre-RC formation; once pre-RCs have formed, Clb2 can no longer inhibit initiation. Paper-1363850.
To allow cell cycle progression, Clb2 proteolysis is triggered by Cdc20 during the metaphase-to-anaphase (M-A) transition and by Hct1 during mitotic exit and G1 [1-6]. Paper-8894702.
In budding yeast, G1 cyclins such as CLN1 and CLN2 are expressed in G1 and S phases, while mitotic cyclins such as CLB1 and CLB2 are expressed in G2 and M phases. Paper-101863.
However, constitutive CLB2 expression does not suppress the mitotic defect, and therefore other essential activities required for the G2-to-M transition must also depend on Mcm1 function. Paper-381186.
This aberrant regulation may be due to aberrant expression of the transcription factors Swi5 and Ace2, which are members of the CLB2 cluster and controllers of the SIC1 cluster. Paper-8402851.
Hypertonic stress causes a decrease in CLB2 mRNA, phosphorylation of Cdc28p, and inhibition of Clb2p- Cdc28p kinase activity, whereas Clb2 protein levels are unaffected. Paper-8814594.
When arrested in late mitosis, the mutants exhibit a defect in cyclin-specific APC activity that is accompanied by high Clb2 levels and low levels of the anaphase inhibitor Pds1. Paper-1623189.
These data show that PKA pathways regulate mitotic progression through Cdc20 and support the DNA damage checkpoint pathways in regulating the destruction of Clb2 and securin. Paper-10204591.
CDK interaction with the NTD of Cdc6 is mediated by the cyclin subunit Clb2, and could be reconstituted with recombinant Clb2 protein and synthetic NTD peptides. Paper-10604625.
Nevertheless, lethality of cdc28-4 clb5 diploids was not rescued by CLB2 or CLB4 overexpression, indicating a specificity of Clb5 function beyond temporality of expression. Paper-1610349.
Here we show that telomerase-negative cells require Clb2 (the major B-type cyclin in this organism), in association with Cdc28 ( Cdk1), to generate postsenescence survivors at a normal rate. Paper-10042113.
Like the morphogenesis checkpoint, the osmotic stress-induced G2 delay is dependent upon the kinase Swe1p, but is not tightly correlated with inhibition of Clb2p- Cdc28p kinase activity. Paper-8814594.
In yeast, a transcription factor, Mcm1, in cooperation with an uncloned factor SFF, regulates the cell cycle-dependent promoter activation of mitotic B-type cyclin genes, CLB1 and CLB2. Paper-8521027.
A mutation in Cdc28 (cdc28-1N) that interferes with Cks1 binding, or inactivation of Cks1 itself, confers stabilization of Clb2, the principal mitotic B-type cyclin in budding yeast. Paper-1850520.
Saccharomyces Wee1 (Swe1) inhibits Cdc28 ( Cdk1) associated with the mitotic cyclin, Clb2, but not with the G(1) ( Cln1, -2, and -3) or the S-phase ( Clb5 and -6) cyclins. Paper-12836884.
In the absence of NAP1, Clb2 is unable to efficiently induce mitotic events, and cells undergo a prolonged delay at the short spindle stage with normal levels of Clb2/p34CDC28 kinase activity. Paper-299608.
Here we compare the specificity of two budding yeast cyclins, the S-phase cyclin Clb5 and the M-phase cyclin Clb2, in the phosphorylation of 150 Cdk1 ( Cdc28) substrates. Paper-11170084.
This defect appears to be caused by a decrease in the binding of Cdc28 and Cln2. cdc37-1 mutants also exhibit a defect in the binding and activation of Cdc28 by the mitotic cyclin Clb2. Paper-230345.
Swe1 and Clb2 are also involved in this form of differentiation, and the core status of Swe1/ Clb2/ Cdc28 in the mechanism of filamentous differentiation has therefore been confirmed. Paper-10117658.
The ' CLB2' cluster contains 33 genes whose transcription peaks early in mitosis, including CLB1, CLB2, SWI5, ACE2, CDC5, CDC20 and other genes important for mitosis. Paper-8402851.
Taken together, these analyses suggest that CLB1 and CLB2 are crucial for mitotic induction, whereas CLB3 and CLB4 might participate additionally in DNA replication and spindle assembly. Paper-75072.
Temperature-sensitive rsi1/ apc2 mutants arrest in metaphase and are unable to degrade Clb2p, suggesting that Rsi1p/ Apc2p is associated with the anaphase promoting complex (APC). Paper-1316691.
Clb2- Cdc28 also facilitated Cdc5 localization to the bud neck through the enhanced interaction between the Clb2-Cdc28- phosphorylated Swe1 and the polo-box domain of Cdc5. Paper-10771306.
We propose that chromatin-mediated repression by Isw1 and Isw2 may serve to limit activation of CLB2 expression by the Clb2/Cdk1 kinase during G(2)/M and to fully repress expression during G(1). Paper-12479992.
In vivo, S phase-promoting Clb5p/ Cdc28p complexes were phosphorylated more slowly and dephosphorylated more effectively than were mitosis- promoting Clb2p/ Cdc28p complexes. Paper-13342115.
CLB1 and CLB2 mRNA levels peak late in the cell cycle, whereas CLB3 and CLB4 are expressed earlier in the cell cycle but peak later than the G1-specific cyclin, CLN1. Paper-75072.
We tested Cdh1 overexpression and the deletion of CLB2 (mitotic cyclin, substrate of APC/ Cdh1) and found that both mutations had a rescuing effect on the expanded polyglutamine toxicity. Paper-13499248.
Therefore, Clb2 cannot drive timely activation of either early or late replication origins, demonstrating that Clb2-directed CDK has a specificity distinct from that driven by Clb5 and Clb6. Paper-8556620.
In contrast, our results demonstrate that the Clb2- Cdc28 cyclin-dependent kinase complex controls specific cell-cycle events through a pathway that involves a GTPase and at least two different kinases. Paper-1637511.
In contrast, Clb2- associated H1 kinase and Cdc28 binding was normal in immunoprecipitates from these cells. cdc28-csr1 was significantly deficient in other aspects of genetic interaction with Cln2. Paper-1274582.
The proline-directed phosphatase, Cdc14p, is a key component of MEN and promotes mitotic exit by activating the degradation of Clb2p and by reversing Cdk-mediated mitotic phosphorylation. Paper-11534399.
Remarkably, elevated levels of Hct1 ectopically activate destruction box- and Cdc23-dependent degradation of Clb2 and cause phenotypic effects characteristic for a depletion of M-phase cyclins. Paper-1169436.
The post-translational mobility shift can be generated in vitro by incubation of Ste20p with immunoprecipitated Cln2p kinase complexes, but not by immunoprecipitated Clb2p or Clb5p kinase complexes. Paper-1610584.
Furthermore, the deletion of XBP1 prevents the drop in Clb2 levels and inhibits cellular elongation in nitrogen-limited chemostat cultures as well as inhibiting pseudohyphal growth on nitrogen-limited agar media. Paper-8778768.
A point mutation in a potential leucine-rich nuclear export signal (NES) enhances the nuclear localization of the protein, and delta- yrb2 cells exhibit an apparent Clb2p nuclear export defect. Paper-8733593.
Pds1p proteolysis precedes that of Clb2p by at least 15 min, which helps to ensure that cells never re-replicate their genome before they have separated sister chromatids at the previous mitosis. Paper-1371781.
Mutation of Clb2 residues N260 and K270 largely abrogates Clb2- Cdc28 regulation by Swe1, and reciprocal mutation of the corresponding residues in Clb5 can subject Clb5- Cdc28 to regulation by Swe1. Paper-12836884.
In vivo footprinting experiments show that Mcm1, in conjunction with an Mcm1-recruited factor, binds to the promoter regions of SWI5 and CLB2 at sites shown to be involved in cell cycle regulation. Paper-381186.
Our results support a model in which cytoplasmic Clb2- Cdk1 is required for timely inactivation of Swe1 at the G2/M transition and bud neck targeting of Clb2 contributes to the efficiency of this process. Paper-12372762.
Ubc11p does not ubiquitinate cyclin B in clam cell-free extracts in vitro and the destruction of Clb2p is not impaired in extracts prepared from delta ubc11 or delta ubc4 delta ubc11 cells. Paper-1583060.
Phosphorylation of Clb5-specific targets during S phase was reduced by replacing Clb5 with Clb2 or by mutating the substrate RXL motif, confirming the importance of Clb5 specificity in vivo. Paper-11170084.
Conversely, deletion of the mitogen-activated protein kinase HOG1 does prevent Clb2p- Cdc28p inhibition by hypertonic stress, but does not block Cdc28p phosphorylation or alleviate the cell cycle delay. Paper-8814594.
Two new B-type cyclin genes from Saccharomyces cerevisiae, called CLB5 and CLB6, are located in a tail to tail arrangement adjacent to the G2/ M phase promoting cyclins CLB2 and CLB1, respectively. Paper-106530.
Correlating with this phenotype, bud3(Delta1221) cells exhibit a pronounced (15-30 minutes) delay in cytokinesis and/or cell separation, suggesting an unanticipated function of Clb2 in these late mitotic events. Paper-9984159.
In budding yeast, a protein called Nap1 binds to the mitotic cyclin Clb2, and Nap1 is required for the ability of Clb2 to induce specific mitotic events, but the role played by Nap1 is unclear. Paper-1111925.
Sporulation experiments on strains deleted for one, two, or three Clbs indicate, in agreement with the biochemical data, that Clb1 is the primary cyclin for the regulation of meiosis, while Clb2 is not involved at all. Paper-85772.
The transition from low to high Clb2-dependent kinase activity is driven by transient activation of Cln2-dependent kinase, and the reverse transition is driven by transient activation of the Clb2 degradation machinery. Paper-10614692.
Taken together, our data uncover a new role for Bud3 in cytokinesis that correlates with its capacity to target Clb2 at the neck, independently of its well established cell-type-specific function in bud site selection. Paper-9984159.
We show that the inactivation of PKA or expression of phosphorylation-defective Cdc20 proteins accelerates securin and Clb2 destruction in chk1 mutants and is sufficient to remove most of the DNA damage-induced delay. Paper-10204591.
The Mcm1p- Fkh2p complex, in combination with the coactivator Ndd1p, plays an important role in the cell cycle-dependent expression of the CLB2 gene cluster during the G2 and M phases ([4-7]; see [8-10]for reviews). Paper-10181049.
CDK activity affects Cdc6 function by multiple mechanisms: CDK activity affects transcription of CDC6, degradation of Cdc6, nuclear import of Cdc6, and binding of Cdc6 to Clb2. Paper-12478287.
Our experiments also suggest that NAP1 is required for the ability of the Clb2/p34CDC28 kinase complex to amplify its own production, and that NAP1 plays a role in regulation of microtubule dynamics during mitosis. Paper-299608.
In separate experiments, designed to examine the effects of inducing either the G1 cyclin Cln3p or the B-type cyclin Clb2p, we found that the mRNA levels of more than half of these 800 genes respond to one or both of these cyclins. Paper-1705556.
The forkhead transcription factor Fkh2p acts in a DNA- bound complex with Mcm1p and the coactivator Ndd1p to regulate cell cycle-dependent expression of the CLB2 gene cluster in Saccharomyces cerevisiae. Paper-10604593.
The MADS-box transcription factor Mcm1p and forkhead (FKH) transcription factor Fkh2p act in a DNA- bound complex to regulate cell-cycle dependent expression of the CLB2 cluster in Saccharomyces cerevisiae. Paper-9663606.
We have found that the essential Reb1 transcription factor binds with high affinity to a sequence upstream of CLB2, within a region implicated previously by others in regulated expression, but upstream of the known G2/M-specific site. Paper-9783876.
This cell cycle arrest can be overcome and partial suppression of the ts phenotype of rts1-null cells occurs if the gene CLB2, encoding a Cdc28 kinase-associated B-type cyclin, is expressed on a high-copy-number plasmid. Paper-1027308.
Cell cycle-regulated transcription of CLB2 in the G2/ M phase is known to be brought about by a set of proteins including Mcm1p, Fkh2/1p and Ndd1p that associate with a 35 bp G2/M-specific sequence common to a set of co-regulated genes. Paper-9783876.
These results demonstrate that the activation of Gin4 is under the control of Clb2 and Nap1, and they provide an important step towards elucidating the molecular pathways that link cyclin-dependent kinases to the events they control. Paper-1111925.
Here we show that this relationship between anaphase-promoting complex (APC) and Clb proteins is reversed in S phase such that the early Clb kinases ( Clb3, Clb4, and Clb5 kinases) inactivate APC(Hct1) to allow Clb2 accumulation. Paper-9011353.
Coexpression of truncated Rts1p and high levels of Clb2p fully suppresses the ts phenotype, indicating that the inhibition of growth of rts1-null cells at high temperatures is due to both stress-related and cell cycle-related defects. Paper-1027308.
This defect was not suppressed by deletion of CLB2, which is involved in switching from polar to isotropic bud growth, indicating that the observed phenotype is not the result of Whi3 acting solely as a negative regulator of cyclin Clb2. Paper-13813359.
In fact, overexpression of CLB2 is toxic when ROT1 is partially inactivated, and reciprocally, deletion of CLB2 suppresses the lethality of the rot1 mutant, which indicates a functional antagonism between Clb2 and Rot1. Paper-13322897.
Although we did not identify any highly Clb2-specific substrates, we found that Clb2- Cdk1 possessed higher intrinsic kinase activity than Clb5- Cdk1, enabling efficient phosphorylation of a broad range of mitotic Cdk1 targets. Paper-11170084.
Using specific clb deletion mutants and plasmid or genomic HA epitope-tagged CLBs, we show that one of these complexes is composed almost exclusively (93% or greater) of Clb2p- Cdc28p, whereas the other is mainly (75% or greater) Clb3p- Cdc28p. Paper-1911441.
Furthermore, we find that inactivation of Cln- and Clb- Cdc28 kinases is sufficient to trigger Clb2 proteolysis and sister-chromatid separation in G2/M phase-arrested cells, where the B-type cyclin-specific proteolysis machinery is normally inactive. Paper-1046780.
We discuss the possibility that the CLB2 gene is coregulated with other genes known to be regulated with the same periodicity and suggest that Mcm1 and the ternary complex factor may coordinately regulate several other G2-regulated transcripts. Paper-240970.
Destruction of the anaphase inhibitor Pds1p is necessary for separation of sister chromatids, whereas destruction of the mitotic cyclin Clb2p is important for disassembly of the mitotic spindle, cytokinesis and re-replication of the genome. Paper-1371781.
We identified a complex array of genetic interactions among these mutants and found that the growth defect in most of the mutants is suppressed by overexpression of SPO12, YAK1, and SIC1 and is exacerbated by overproduction of the mitotic cyclin Clb2. Paper-1623189.
CLB5::CLB2 exhibited almost no rescue of clb5-specific replication defects, although it could rescue clb1 clb2 lethality, and in synchronized cells Clb2p-associated kinase activity from CLB5::CLB2 rose early in the cell cycle, similar to that of Clb5p. Paper-1951184.
G1-specific cyclins encoded by CLN1, CLN2, and CLN3 are required for entry into the cell cycle (Start) and thereby for S phase, whereas G2-specific B-type cyclins encoded by CLB1, CLB2, CLB3, and CLB4 are required for mitosis. Paper-94143.
A point mutation in the CLB2 UAS which blocked ternary complex formation, but still allowed Mcm1 to bind, resulted in loss of cell cycle regulation in vivo, suggesting that the ternary complex factor is also important in control of CLB2 transcription. Paper-240970.
In agreement with the idea that cdc14 mutations elevate Clb- Cdc28 kinase activity, deletion of the gene for the Clb- Cdc28 inhibitor Sic1 caused synthetic lethality with cdc14-1, as did the deletion of HCT1, which is required for proteolysis of Clb2p. Paper-2152209.
The clb2 cdc14 strains arrested with replicated but unseparated DNA and unseparated spindle pole bodies; this phenotype is distinct from the late mitotic arrest of the sic1::TRP1 cdc14-1 and the cdc14-1 hct1::LEU2 double mutants and of the cdc14 CLN2 overexpressor. Paper-2152209.
Together, these results demonstrate that NAP1 is required for the normal function of the activated Clb2/p34CDC28 kinase complex, and provide a step towards understanding how cyclin-dependent kinase complexes induce specific events during the cell cycle. Paper-299608.
We showed that accumulation of CLB2 transcripts in G2 cells is controlled at the transcriptional level and identified a 55-bp upstream activating sequence (UAS) containing an Mcm1 binding site as being necessary and sufficient for cell cycle regulation. Paper-240970.
We present evidence that strongly suggests that Cdc20 is an essential regulator of APC-dependent proteolysis such that in the absence of Cdc20, cells are unable to degrade either Pds1 at the onset of anaphase or the mitotic cyclin Clb2 during telophase. Paper-1401489.
Cdc15p is an essential protein kinase and functions with a group of late mitotic proteins that includes Lte1p, Tem1p, Cdc14p and Dbf2p/ Dbf20p to inactivate Cdc28p- Clb2p at the end of mitosis in budding yeast [1] [2]. Paper-8351046.
Prolonging polarized growth phases by disrupting the G(2)/M cyclin gene CLB2 enhances the accuracy of bud site selection in wild-type, spa2Delta, and ste20Delta cells, whereas shortening the polarized growth phases by deleting SWE1 decreases the fidelity of bipolar budding. Paper-8395421.
Swe1 phosphorylation by Clb2- Cdc28, which is thought to activate Swe1 kinase, depends on N260 and K270, suggesting that specific regulation of Clb2- Cdc28 by Swe1 derives from the specific ability of Clb2 to target Swe1 for activating phosphorylation. Paper-12836884.
Because the cell cycle machinery participates in Saccharomyces cerevisiae filamentous growth, we characterized in detail the two C. albicans B-type cyclins, CLB2 and CLB4, to better understand the molecular mechanisms that underlie the C. albicans morphogenic switch. Paper-11096433.
Interestingly, deletions in either FKH1 or FKH2 alone caused subtle but opposite effects on cell-cycle progression and CLB2 mRNA expression, consistent with a role for each of these genes in modulating the cell cycle and having opposing effects on silencing. Paper-8359820.
In the yeast Saccharomyces cerevisiae, the MADS-box protein Mcm1, which is highly related to mammalian SRF (serum response factor), forms a ternary complex with SFF (Swi five factor) to regulate the cell cycle expression of genes such as SWI5, CLB2 and ACE2. Paper-8425525.
We show here that CLB2 proteolysis, which is important for transition from mitosis to G1, is not confined to a narrow window at the end of mitosis as previously thought but continues until reactivation of CDC28 by CLN cyclins toward the end of the subsequent G1 period. Paper-125310.
The stable association of Swe1 with Clb2- Cdc28 also depends on these residues, suggesting that Swe1 may competitively inhibit Clb2- Cdc28 interactions with substrates, in addition to its well-known function as a regulator of CDK activity through tyrosine phosphorylation. Paper-12836884.
In particular, we find that Cdc5p is temporally recruited to promoters of the cell-cycle- regulated CLB2 gene cluster, where it targets the Mcm1p- Fkh2p- Ndd1p transcription factor complex, through direct phosphorylation of the coactivator protein Ndd1p. Paper-12329497.
Thus, genes that are co-induced during G1/S of the mitotic cell cycle, the dynamics of the septin Cdc10 and the kinetics of accumulation of the cyclin Clb2 all exhibit distinct patterns of regulation during spore germination, which allow the separation of cell growth from nuclear events. Paper-13453954.
Furthermore, the ability of Swe1 to inhibit the activity of different B-type cyclins in replication initiation correlates with the normal expression timing of those cyclins, with no apparent in vivo inhibition of Clb5 and Clb6, moderate inhibition of Clb3 and Clb4, and strong inhibition of Clb2. Paper-11126644.
Because conserved cell cycle regulators, the mitotic cyclin-dependent kinase Clb2/ Cdc28, and its inhibitor Swe1 were found to be involved in both nitrogen starvation- and short chain alcohol-induced filamentous differentiation, they were identified as components of the core mechanism for filamentous differentiation. Paper-10117658.
This study shows that the combination of early cell cycle expression and deletion of the CDK inhibitor Saccharomyces Wee1 ( Swe1) enables the mitotic B-type (Clb) cyclins Clb2, Clb3, and Clb4 of Saccharomyces cerevisiae to initiate S phase with similar effectiveness as the S-phase cyclin Clb5. Paper-11126644.
Mutations in three other genes ( GIN4, encoding a kinase related to the Schizosaccharomyces pombe mitotic inducer Nim1p; CLA4, encoding a p21-activated kinase; and NAP1, encoding a Clb2p-interacting protein) also produce perturbations of septin organization associated with an Swe1p-dependent cell cycle delay. Paper-8457327.
With a temperature-sensitive mutant of the CDC23 subunit of the anaphase-promoting complex (APC), cdc23(ts); a temperature-sensitive mutant of cdc20; and a cdh1-null mutant, we show that the diminution of Pds1p and Clb2p brought on by Tax is mediated via the Cdc20p-associated anaphase-promoting complex, APC(Cdc20p). Paper-9796384.
On hyphal induction, the accumulation of the G1 cyclin Cln1p was prolonged, whereas the accumulation of both Clb proteins was delayed when compared with yeast form cells, indicating that CLB2 and CLB4 are differentially regulated in the two morphologies and that the dynamics of cyclin appearance differs between yeast and hyphal forms of growth. Paper-11096433.
These synonyms are used for gene CLB2 (B-type cyclin involved in cell cycle progression; activates Cdc28p to promote the transition from G2 to M phase; accumulates during G2 and M, then targeted via a destruction box motif for ubiquitin...): YPR119W, P9642.6, G2/mitotic-specific cyclin-2.
These accession numbers are used for gene CLB2: CAA44195 (NCBI_GENBANK__AC), AAA34502 (NCBI_GENBANK__AC).
CLB2 is a homologue of NCU02758 (G2/mitotic-specific cyclin-B) from Neurospora crassa OR74A.
CLB2 is a homologue of MGG_05646 (hypothetical protein) from Magnaporthe grisea 70-15.
CLB2 is a homologue of LOC608420 (similar to G2/mitotic-specific cyclin B1) from Canis lupus familiaris.
CLB2 is a homologue of LOC485338 (similar to G2/mitotic-specific cyclin B1) from Canis lupus familiaris.
CLB2 is a homologue of KLLA0D15543g (hypothetical protein) from Kluyveromyces lactis NRRL Y-1140.
CLB2 is a homologue of Gm5593 (predicted gene 5593) from Mus musculus.
CLB2 is a homologue of CYCB1;3 (CYCB1;3 (CYCLIN B1;3); cyclin-dependent protein kinase regulator) from Arabidopsis thaliana.
CLB2 is a homologue of CYCB1;1 (CYCB1;1 (CYCLIN B1;1); cyclin-dependent protein kinase regulator) from Arabidopsis thaliana.
CLB2 is a homologue of CycB (Cyclin B) from Drosophila melanogaster.
CLB2 is a homologue of CYC1BAT (CYC1BAT; cyclin-dependent protein kinase regulator) from Arabidopsis thaliana.
CLB2 is a homologue of cdc13 (cyclin Cdc13) from Schizosaccharomyces pombe.
CLB2 is a homologue of CCNB1 (cyclin B1) from Homo sapiens.
CLB2 is a homologue of CCNB1 (cyclin B1) from Bos taurus.
CLB2 is a homologue of CCNB1 (cyclin B1) from Pan troglodytes.
CLB2 is a homologue of Ccnb1 (cyclin B1) from Mus musculus.
CLB2 is a homologue of Ccnb1 (cyclin B1) from Rattus norvegicus.
CLB2 is a homologue of ccnb1 (cyclin B1) from Danio rerio.
CLB2 is a homologue of AGOS_AAR099W (AAR099Wp) from Ashbya gossypii ATCC 10895.
CLB2 is a homologue of AgaP_AGAP004963 (AGAP004963-PA) from Anopheles gambiae str. PEST.
CLB2 is a homologue of AgaP_AGAP004962 (AGAP004962-PA) from Anopheles gambiae str. PEST.
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