Components of the spindle-assembly checkpoint are essential in Caenorhabditis elegans

Kitagawa, Risa; Rose, Ann M.

doi:10.1038/70309

Cited by 127 publications

(176 citation statements)

References 48 publications

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“…Our studies show that either Mad2⌬C or GST-Mad1F10 can overcome the checkpoint in nocodazole-treated PtK1 cells where kinetochores lack both tension as well as attached microtubules. This result indicates that BubR1 is not able to maintain the spindle checkpoint independently of Mad2 function, a conclusion supported by other studies where Mad2 function was inhibited with antibodies or deleted by genetic manipulations [Canman et al, 2000;Dobles et al, 2000;Gorbsky et al, 1998;Hoyt, 2001;Kitagawa and Rose, 1999;Li and Murray, 1991;Li and Benezra, 1996;Michel et al, 2001;Waters et al, 1998]. How the kinetochore mediates inhibition of APC/C by Cdc20 via Mad2, BubR1, or a direct effect on APC/C remains an important unresolved issue [Gillett and Sorger, 2001;Hoyt, 2001;Sudakin et al, 2001].…”

Section: Comments and Conclusionmentioning

confidence: 70%

Inducing precocious anaphase in cultured mammalian cells

Canman

Salmon

Fang

2002

Cell Motil. Cytoskeleton

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The spindle checkpoint, which prevents anaphase onset upon spindle damage or incorrect chromosome alignment, presents a problem for experimental analysis of protein function in anaphase and cytokinesis. This is because the functional disruption of many proteins before anaphase onset can activate this checkpoint, preventing anaphase and subsequent cell cycle events. This paper compares new and old methods of overriding the spindle checkpoint in prometaphase mammalian tissue culture cells. Cell Motil. Cytoskeleton 52:61–65, 2002. © 2002 Wiley‐Liss, Inc.

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Section: Comments and Conclusionmentioning

confidence: 70%

Inducing precocious anaphase in cultured mammalian cells

Canman

Salmon

Fang

2002

Cell Motil. Cytoskeleton

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“…Mutation of Drosophila bub1 [Basu et al, 1999] or deletion of mad2 in mice [Dobles et al, 2000] or C. elegans [Kitagawa and Rose 1999] promotes chromosome mis-segregation and early embryonic lethality. These results suggest that the spindle checkpoint regulates mitotic timing in every cell cycle, an idea that is supported by experiments demonstrating that impaired function of Mad2p or Mad3p/BubR1p accelerates mitotic progression Meraldi et al, 2004a].…”

Section: The Spindle Checkpoint Is Required For Accurate Chromosome Smentioning

confidence: 99%

SAC‐ing mitotic errors: How the spindle assembly checkpoint (SAC) plays defense against chromosome mis‐segregation

Kadura

Sazer

2005

Cell Motil. Cytoskeleton

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“…In Caenorhabditis elegans, homologues of MAD1 and MAD2, called mdf-1 and mdf-2, are required for viability and promote the arrest of mitotically proliferating premeiotic germ cells exposed to nocodazole (Kitagawa and Rose, 1999 …”

Section: Introductionmentioning

confidence: 99%

“…CENP-F levels are increased at unaligned kinetochores during meiosis in mouse spermatocytes, leading to suggestions that CENP-F might play a role in meiotic spindle checkpoint signaling (Eaker et al, 2001). It is not clear, however, what role, if any, CENP-F has in mitotic checkpoint signaling.In Caenorhabditis elegans, homologues of MAD1 and MAD2, called mdf-1 and mdf-2, are required for viability and promote the arrest of mitotically proliferating premeiotic germ cells exposed to nocodazole (Kitagawa and Rose, 1999 …”

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confidence: 99%

A Spindle Checkpoint Functions during Mitosis in the EarlyCaenorhabditis elegansEmbryo

Encalada

Willis

Lyczak

et al. 2005

MBoC

118

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During mitosis, chromosome segregation is regulated by a spindle checkpoint mechanism. This checkpoint delays anaphase until all kinetochores are captured by microtubules from both spindle poles, chromosomes congress to the metaphase plate, and the tension between kinetochores and their attached microtubules is properly sensed. Although the spindle checkpoint can be activated in many different cell types, the role of this regulatory mechanism in rapidly dividing embryonic animal cells has remained controversial. Here, using time-lapse imaging of live embryonic cells, we show that chemical or mutational disruption of the mitotic spindle in early Caenorhabditis elegans embryos delays progression through mitosis. By reducing the function of conserved checkpoint genes in mutant embryos with defective mitotic spindles, we show that these delays require the spindle checkpoint. In the absence of a functional checkpoint, more severe defects in chromosome segregation are observed in mutants with abnormal mitotic spindles. We also show that the conserved kinesin CeMCAK, the CENP-F-related proteins HCP-1 and HCP-2, and the core kinetochore protein CeCENP-C all are required for this checkpoint. Our analysis indicates that spindle checkpoint mechanisms are functional in the rapidly dividing cells of an early animal embryo and that this checkpoint can prevent chromosome segregation defects during mitosis. INTRODUCTIONDuring mitosis, some microtubules emanating from bipolar microtubule organizing centers grow toward chromosomes and attach to specialized chromosomal regions called kinetochores (Skibbens and Hieter, 1998;Cleveland et al., 2003). Once captured, sister chromatids are segregated, one to each of two daughter cells. Eukaryotic cells have evolved a mechanism called the spindle checkpoint, to monitor chromosomal segregation and increase the fidelity of mitosis (reviewed in Gardner and Burke, 2000;McIntosh et al., 2002). Until spindle microtubules from both poles capture and align all sister chromatid pairs at a metaphase plate, the spindle checkpoint produces a delay in the onset of anaphase. If this delay is bypassed by reducing checkpoint function, anaphase starts prematurely, and daughter cells may receive unequal complements of chromosomes. Such genomic instability can result in lethality and in tumorigenesis (Hartwell and Kastan, 1994;Basu et al., 1999).Originally identified and characterized in Saccharomyces cerevisiae, seven spindle assembly checkpoint genes (MAD1, MAD2, MAD3, BUB1, BUB2, BUB3, and MPS1) are known to function at kinetochores to inhibit anaphase onset, or to mediate mitotic exit in the presence of spindle abnormalities (Hoyt et al., 1991;Li and Murray, 1991). Mutations in these genes reduce or eliminate the cell cycle delays that normally occur after treatment with microtubule depolymerizing drugs (Wang and Burke, 1995;Pangilinan and Spencer, 1996). Bub1 and Bub3 form a protein kinase complex that, in concert with Mps1, functions at kinetochores upstream of Mad1 and Mad2 (Roberts et al., 1994;H...

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Components of the spindle-assembly checkpoint are essential in Caenorhabditis elegans

Cited by 127 publications

References 48 publications

Inducing precocious anaphase in cultured mammalian cells

Inducing precocious anaphase in cultured mammalian cells

SAC‐ing mitotic errors: How the spindle assembly checkpoint (SAC) plays defense against chromosome mis‐segregation

A Spindle Checkpoint Functions during Mitosis in the EarlyCaenorhabditis elegansEmbryo

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