Differential function and expression of Saccharomyces cerevisiae B-type cyclins in mitosis and meiosis.

Grandin, Nathalie; Reed, Steven I.

doi:10.1128/mcb.13.4.2113

Cited by 159 publications

(164 citation statements)

References 88 publications

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“…As was shown in previous works (20,21), successful transition from G 2 into mitosis depends on Cdc28p (Cdk1p) activity, which in turn is activated by B-type cyclins Clb1p and Clb2p. A decreased level of these cyclins arrests cells in G 2 /M phase with an elongated-bud phenotype.…”

Section: Cyclinb1 Protein Level Was Decreased In Translocantsmentioning

confidence: 95%

“…According to previous works (20,27), a decreased Clb1p level suggests that the majority of translocants had impairments in the completion of the S phase of the cell cycle. Besides the DSBs necessary for the homologous DNA integration, translocations produced some DNA damage, most likely DSBs mimicked by the free DNA ends of the telomeric fragments that eventually were recovered by ectopic integration on chromosome XI (Fig.…”

Section: Discussionmentioning

confidence: 99%

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Cellular and molecular effects of nonreciprocal chromosome translocations in Saccharomyces cerevisiae

Nikitin

Tosato²,

Zavec³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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Saccharomyces cerevisiae strains harboring a nonreciprocal, bridgeinduced translocation (BIT) between chromosomes VIII and XV exhibited an abnormal phenotype comprising elongated buds and multibudded, unevenly nucleated pseudohyphae. In these cells, we found evidence of molecular effects elicited by the translocation event and specific for its particular genomic location. Expression of genes flanking both translocation breakpoints increased up to five times, correlating with an increased RNA polymerase II binding to their promoters and with their histone acetylation pattern. Microarray data, CHEF, and quantitative PCR confirmed the data on the dosage of genes present on the chromosomal regions involved in the translocation, indicating that telomeric fragments were either duplicated or integrated mostly on chromosome XI. FACS analysis revealed that the majority of translocant cells were blocked in G1 phase and a few of them in G2. Some cells showed a posttranslational decrease of cyclin B1, in agreement with elongated buds diagnostic of a G2/M phase arrest. The actin1 protein was in some cases modified, possibly explaining the abnormal morphology of the cells. Together with the decrease in Rad53p and the lack of its phosphorylation, these results indicate that these cells have undergone adaptation after checkpointmediated G2/M arrest after chromosome translocation. These BIT translocants could serve as model systems to understand further the cellular and molecular effects of chromosome translocation and provide fundamental information on its etiology of neoplastic transformation in mammals.DNA integration ͉ yeast ͉ genome expression ͉ genome dynamics ͉ transcription

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Section: Cyclinb1 Protein Level Was Decreased In Translocantsmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Cellular and molecular effects of nonreciprocal chromosome translocations in Saccharomyces cerevisiae

Nikitin

Tosato²,

Zavec³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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“…It has been proposed that some checkpoint controls over mitosis are switched from the APC/C during G1 to include tyrosine phosphorylation of p34 cdc2 upon initiation of DNA replication (Ye et al, 1997a). BIME APC1 may therefore normally play a role to prevent activation of NIMA kinase, and other mitotic regulators, during interphase to prevent premature mitosis.The levels of NIME cyclinB and NIMA proteins oscillate once each cell cycle in a strikingly similar manner (Evans et al, 1983;Alfa et al, 1990;Draetta et al, 1990;Ghiara et al, 1991;Hunt et al, 1992;Richardson et al, 1992;Grandin and Reed, 1993;Pu and Osmani, 1995;Ye et al, 1995;Yamano et al, 1996). Both proteins accumulate during late S to G2, peak at early M, and are rapidly degraded as cells progress out of mitosis with slightly different kinetics Ye et al, 1995).…”

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confidence: 95%

Regulation of the Anaphase-promoting Complex/Cyclosome bybimA^APC3and Proteolysis of NIMA

Fincher

Tang

et al. 1998

MBoC

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Surprisingly, although highly temperature-sensitive, the bimA1 APC3 anaphase-promoting complex/cyclosome (APC/C) mutation does not cause arrest of mitotic exit. Instead, rapid inactivation of bimA1 APC3 is shown to promote repeating oscillations of chromosome condensation and decondensation, activation and inactivation of NIMA and p34 cdc2 kinases, and accumulation and degradation of NIMA, which all coordinately cycle multiple times without causing nuclear division. These bimA1 APC3 -induced cell cycle oscillations require active NIMA, because a nimA5 ϩ bimA1 APC3 double mutant arrests in a mitotic state with very high p34 cdc2 H1 kinase activity. NIMA protein instability during S phase and G2 was also found to be controlled by the APC/C. The bimA1 APC3 mutation therefore first inactivates the APC/C but then allows its activation in a cyclic manner; these cycles depend on NIMA. We hypothesize that bimA APC3 could be part of a cell cycle clock mechanism that is reset after inactivation of bimA1 APC3 . The bimA1 APC3 mutation may also make the APC/C resistant to activation by mitotic substrates of the APC/C, such as cyclin B, Polo, and NIMA, causing mitotic delay. Once these regulators accumulate, they activate the APC/C, and cells exit from mitosis, which then allows this cycle to repeat. The data indicate that bimA APC3 regulates the APC/C in a NIMA-dependent manner. INTRODUCTIONThe bimE and bimA genes were originally defined by temperature-sensitive mutations in functions required for normal progression through mitosis in Aspergillus nidulans (Morris, 1976;Osmani et al., 1988;Engle et al., 1990;O'Donnell et al., 1991) and were subsequently found to encode highly conserved proteins whose homologues have been isolated from many organisms ranging from fungi to humans (Hirano et al., 1990(Hirano et al., , 1994Mirabito and Morris, 1993;Lamb et al., 1994;Starborg et al., 1994;King et al., 1995;. Most significantly, they were recently identified as components of the anaphase-promoting complex (APC) (King et al., 1995;Peters et al., 1996;. The APC is also known as the cyclosome and is therefore abbreviated here to APC/C (see Townsley and Ruderman, 1998, for review).bimE encodes the largest subunit of the APC/C and has recently been termed APC1 . We will use the designation bimE APC1 for the gene and BIME APC1 for the protein. bimA encodes a member of the tetratricopeptide repeat family of proteins, being most similar to Schizosaccharomyces pombe nuc2 (Hirano et al., 1990(Hirano et al., , 1994 and Saccharomyces cerevisiae CDC27 (Sikorski et al., 1990;Lamb et al., 1994), which was recently termed APC3 APC/C functions as an E3 ubiquitin ligase, which specifically targets proteins (such as mitotic cyclins) for degradation in a destruction box (D box)-dependent manner (Glotzer et al., 1991;King et al., 1996b) through the ubiquitin-proteasome pathway, to promote initiation of anaphase and exit from mitosis into G1 (for reviews see Murray, 1995;King et al., 1996a;Hershko, 1997;Townsley and Ruderman, 1998). APC/C activity i...

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“…These extracts were then centrifuged for 15 min at 13,000 g to generate the P13 fraction and the supernatant was centrifuged at 100,000 g to obtain the P100 and the S100 fractions. The HA-tagged Bedl fusion proteins were detected by Western blotting using the 12CA5 monoclonal antibody with the ECL detection kit (Amersham Corp., Arlington Heights, IL) as previously described (Grandin and Reed, 1993). Kar2 was detected with a rabbit serum kindly provided by M. Rose.…”

Section: Protein Analysismentioning

confidence: 99%

BED1, a gene encoding a galactosyltransferase homologue, is required for polarized growth and efficient bud emergence in Saccharomyces cerevisiae.

Mondésert

Reed

1996

The Journal of Cell Biology

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Abstract. The ellipsoidal shape of the yeast Saccharomyces cerevisiae is the result of successive isotropic/apical growth switches that are regulated in a cell cycledependent manner. It is thought that growth polarity is governed by the remodeling of the actin cytoskeleton that is itself under the control of the cell cycle machinery. The cell cycle and the morphogenesis cycle are tightly coupled and it has been recently suggested that a morphogenesis/polarity checkpoint control monitors bud emergence in order to maintain the coupling of these two events (Lew, D. J., and S. I. Reed. 1995. J. Cell BioL 129:739-749). During a screen based on the inability of cells impaired in the budding process to survive when the morphogenesis checkpoint control is abolished, we identified and characterized BED1, a new gene that is required for efficient budding. Cells carrying a disrupted allele of BED1 no longer have the wild-type ellipsoidal shape characteristic of S. cerevisiae, are larger than wild-type cells, are deficient in bud emergence, and depend upon an intact morphogenesis checkpoint control to survive. These cells show defects in polarized growth despite the fact that the actin cytoskeleton appears normal. Our results suggest that Bedl is a type II membrane protein localized in the endoplasmic reticulum. BED1 is significantly homologous to gma12 ÷, a S. pombe gene coding for an et-l,2-galactosyltransferase, suggesting that glycosylation of specific proteins or lipids could be important for signaling in the switch to polarized growth and in bud emergence.T HE ellipsoidal shape of the yeast Saccharomyces cerevisiae reflects cell cycle-regulated polarized growth. At specific times during the cell cycle, cell growth is either isotropic or polarized toward the bud (for review see Lew and Reed, 1995b). A correlation between local deposition of new cell wall components and actin localization has been established (Adams and Pringle, 1984;Kilmartin and Adams, 1984), leading to the proposal that actin directs secretory vesicles to specific regions of the plasma membrane to allow localized cell surface growth during bud initiation and bud growth. During most of the G1 phase, growth is isotropic and cortical actin patches are delocalized throughout the cell. The attainment of a critical cell size and concomitant execution of START lead to the formation of an actin ring at the pre-bud site and the orientation of actin filaments toward this site. Subsequent to START, growth is almost completely restricted to the emerging bud. During bud growth, cortical actin patches are localized to the bud. Initially, bud growth occurs primarily at the distal tip. At some point, though, there is a switch to isotropic growth first in the bud, then also tranAddress all correspondence to S. I. Reed, Department of Molecular Biology, MB7, The Scripps Research Institute, 10666 North Torrey Pines Road, La Jolla, California 92037. Tel.: (619) 554-6188. siently in the mother cell at mitosis. At cytokinesis, the actin cytoskeleton is reorganized and...

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Differential function and expression of Saccharomyces cerevisiae B-type cyclins in mitosis and meiosis.

Cited by 159 publications

References 88 publications

Cellular and molecular effects of nonreciprocal chromosome translocations in Saccharomyces cerevisiae

Cellular and molecular effects of nonreciprocal chromosome translocations in Saccharomyces cerevisiae

Regulation of the Anaphase-promoting Complex/Cyclosome bybimA^APC3and Proteolysis of NIMA

BED1, a gene encoding a galactosyltransferase homologue, is required for polarized growth and efficient bud emergence in Saccharomyces cerevisiae.

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Differential function and expression of Saccharomyces cerevisiae B-type cyclins in mitosis and meiosis.

Cited by 159 publications

References 88 publications

Cellular and molecular effects of nonreciprocal chromosome translocations in Saccharomyces cerevisiae

Cellular and molecular effects of nonreciprocal chromosome translocations in Saccharomyces cerevisiae

Regulation of the Anaphase-promoting Complex/Cyclosome bybimAAPC3and Proteolysis of NIMA

BED1, a gene encoding a galactosyltransferase homologue, is required for polarized growth and efficient bud emergence in Saccharomyces cerevisiae.

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Regulation of the Anaphase-promoting Complex/Cyclosome bybimA^APC3and Proteolysis of NIMA