Budding yeast RSI1/APC2, a novel gene necessary for initiation of anaphase, encodes an APC subunit

Kramer, Kate

doi:10.1093/emboj/17.2.498

Cited by 50 publications

(38 citation statements)

References 45 publications

(119 reference statements)

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“…This suggests that APC/C and SCF might be derived from the same ancestral ubiquitin protein ligase. Apc2 is a member of the cullin family of proteins, which includes the SCF subunit Cdc53 from budding yeast (Kramer et al 1998b;Yu et al 1998;Zachariae et al 1998b). Cdc53's carboxy-terminal 'cullin' domain recruits the E2 enzyme Cdc34 to the SCF (Patton et al 1998), whereas its amino-terminal region binds to Skp1, which in turn binds to proteins that associate with substrates (Bai et al 1996).…”

Section: The Apc/c Core Particle: Scf's Big Brother?mentioning

confidence: 99%

Whose end is destruction: cell division and the anaphase-promoting complex

Zachariae¹,

Nasmyth²

1999

Genes & Development

635

549

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Cell proliferation depends on the duplication of chromosomes followed by the segregation of duplicates (sister chromatids) to opposite poles of the cell prior to cell division (cytokinesis). How cells ensure that chromosome duplication, chromosome segregation, and cell division occur in the correct order and form an immortal reproductive cycle is one of the most fundamental questions in cell biology. Without such coordination, cells would not maintain a constant chromosome number and sexual reproduction as we know and love it would not be possible. A halfhearted cell cycleThe discovery of cyclin-dependent kinases (CDKs) went some way to answering this question. Successive waves of S-and M-phase-promoting CDKs first trigger chromosome duplication (S phase)-then the attachment of the replicated chromosomes to a bipolar spindle (M phase). In animal cells, S phase is induced by Cdk2 bound to S-phase cyclins (E-and A-type) whereas M phase is triggered by Cdk1 associated with mitotic cyclins (A-and B-type). In both fission yeast and budding yeast, S and M phase are induced by a single CDK (Cdk1) bound to Sphase-and M-phase-specific B-type cyclins, respectively. We now understand many of the regulatory mechanisms that activate S-and M-CDKs in the correct order. We also have a robust hypothesis for how cells ensure that no genomic sequence is duplicated more than once during the interval between the onset of S and M phases. Initiation of DNA replication requires two distinct steps: first, prereplicative complexes (pre-RCs) are assembled at future origins of replication, a process that can occur only in the absence of CDK activity. The second step, origin unwinding and the recruitment of replication enzymes, is triggered by CDK activation. Because pre-RC assembly is inhibited by CDK activity, chromosome rereplication requires a CDK cycle, a period of low CDK activity followed by a period of high CDK activity. Having activated S-CDKs in late G 1 , cells maintain high CDK activity until metaphase and this prevents refiring of replication origins.However, several crucial elements were missing from this CDK-dominated view of the cell cycle. Missing was the impetus that causes sister chromatids to separate at the metaphase-to-anaphase transition; the machinery that destroys mitotic cyclins during anaphase; a mechanism for ensuring that sister chromatid separation normally precedes cytokinesis and chromosome reduplication; and an understanding of how events that trigger sister chromatid separation and exit from mitosis also create the conditions that cause the chromosome cycle to be repeated. Insight into all these questions has recently stemmed from the identification of the machinery responsible for degrading mitotic cyclins, a ubiquitin-protein ligase called the anaphase-promoting complex or cyclosome (APC/C). By destroying anaphase inhibitory proteins, the APC/C triggers the separation of sister chromatids; by destroying mitotic cyclins, it creates the low CDK state necessary for cytokinesis and for reforming the pre-RCs c...

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Section: The Apc/c Core Particle: Scf's Big Brother?mentioning

confidence: 99%

Whose end is destruction: cell division and the anaphase-promoting complex

Zachariae¹,

Nasmyth²

1999

Genes & Development

635

549

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“…Cell cultures were analysed for DNA content using a FACScan Becton Dickinson flow cytometer as described previously (Kramer et al, 1998).…”

Section: Cell Biology Protocolsmentioning

confidence: 99%

“…The polyclonal anti-Sic1 antibody described previously (Donovan et al, 1994) was used at a 1:2000 dilution and the monoclonal anti-TAT1 antibody used to detect tubulin was used at 1:1000 dilution. Immunoprecipitation, kinase and phosphatase assays Clb2-associated kinase activity was measured as previously described (Kramer et al, 1998). Briefly, 250 µg extract was incubated with 0.2 µg rabbit anti-Clb2 antibody (Santa Cruz) for 1 hour at 4°C.…”

Section: Cell Biology Protocolsmentioning

confidence: 99%

Spatial regulation of the guanine nucleotide exchange factor Lte1 inSaccharomyces cerevisiae

Jensen¹,

Geymonat²,

Johnson³

et al. 2002

Journal of Cell Science

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In budding yeast, activation of the small Ras-like GTPase Tem1 triggers exit from mitosis and cytokinesis. Tem1 is regulated by Bub2/Bfa1, a two-component GTPase-activating protein (GAP), and by Lte1, a putative guanine nucleotide exchange factor. Lte1 is confined to the bud cortex, and its spatial separation from Tem1 at the spindle pole body (SPB) is important to prevent untimely exit from mitosis. The pathways contributing to Lte1 asymmetry have not been elucidated. Here we show that establishment of Lte1 at the cortex occurs by an actin-independent mechanism, which requires activation of Cdc28/Cln kinase at START and Cdc42, a key regulator of cell polarity and cytoskeletal organisation. This defines a novel role for Cdc42 in late mitotic events. In turn, dissociation of Lte1 from the cortex in telophase depends on activation of the Cdc14 phosphatase. Ectopic expression of Cdc14 at metaphase results in premature dephosphorylation of Lte1 coincident with its release from the cortex. In vitro phosphatase assays confirm that Lte1 is a direct substrate for Cdc14. Our results suggest that the asymmetry in Lte1 localisation is imposed by Cdc28-dependent phosphorylation.Finally, we report a mutational analysis undertaken to investigate intrinsic Lte1 determinants for localisation. Our data suggest that an intrameric interaction between the N-and C-terminal regions of Lte1 is important for cortex association.

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“…6 APC/C is a very large complex of 1.5 MDa and it has over 10 subunits; the core subunits have cullin and Ring-finger domains, which are the markers of E3 ubiquitin ligase. [7][8][9] The Apc2's cullin domain associates with Apc11's Ring-finger domain 3,10,11 and interacts with E2 ligase. 11,12 Without considering the complexity of APC/C, Apc11 itself can perform E3 ligase activity in vitro, indicating that other subunits may not be essential for E3 function.…”

Section: Introductionmentioning

confidence: 99%

Cyclin B3 controls anaphase onset independent of spindle assembly checkpoint in meiotic oocytes

Zhang

Huang

et al. 2015

Cell Cycle

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Cyclin B3 is a relatively new member of the cyclin family whose functions are little known. We found that depletion of cyclin B3 inhibited metaphase-anaphase transition as indicated by a well-sustained MI spindle and cyclin B1 expression in meiotic oocytes after extended culture. This effect was independent of spindle assembly checkpoint activity, since both Bub3 and BubR1 signals were not observed at kinetochores in MI-arrested cells. The metaphase I arrest was not rescued by either Mad2 knockdown or cdc20 overexpression, but it was rescued by securin RNAi. We conclude that cyclin B3 controls the metaphase-anaphase transition by activating APC/C cdc20 in meiotic oocytes, a process that does not rely on SAC activity.

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Budding yeast RSI1/APC2, a novel gene necessary for initiation of anaphase, encodes an APC subunit

Cited by 50 publications

References 45 publications

Whose end is destruction: cell division and the anaphase-promoting complex

Whose end is destruction: cell division and the anaphase-promoting complex

Spatial regulation of the guanine nucleotide exchange factor Lte1 inSaccharomyces cerevisiae

Cyclin B3 controls anaphase onset independent of spindle assembly checkpoint in meiotic oocytes

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