Splitting the Chromosome: Cutting the Ties that Bind Sister Chromatids

Nasmyth, Kim; Jm, Peters; Uhlmann, Frank

doi:10.1002/0470846666.ch10

Cited by 38 publications

(29 citation statements)

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“…Cohesin is combined with the chromosome in the G1 phase and holds the sister chromatids until RAD21 is cleaved by separase during the onset of anaphase, with these cleavages allowing chromosomal separation [9,17,18,24,33]. When RAD21 was knocked out of chicken DT40 cells, it caused premature sister chromatid separation [30].…”

Section: Introductionmentioning

confidence: 99%

Correlation of invasion and metastasis of cancer cells, and expression of the RAD21 gene in oral squamous cell carcinoma

et al. 2006

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Although RAD21 is involved in the repair of double-strand breaks in DNA and is essential for mitotic growth, its role in cancer has been unclear. In this study, the relevance of RAD21 gene expression to the invasion and metastasis of oral squamous cell carcinoma was clarified using laser microdissection and real-time polymerase chain reaction (PCR). Using two different metastatic potential oral squamous cells [high-metastatic-potential squamous cell carcinoma cells (SAS-Ly) and low-metastatic-potential squamous cell carcinoma cells (SAS)], the relation of RAD21 gene expression to apoptosis, invasion, and metastasis was examined. The results showed that RAD21 gene expression was significantly decreased in oral squamous cell carcinoma when it expressed the INFbeta and INFgamma invasion patterns in comparison with the INFalpha invasion pattern (p<0.01). In addition, in comparison with SAS cells, SAS-Ly cells indicated tolerance to cell death induced by an apoptosis induction reagent, while the expression level of the RAD21 gene in SAS cells was increased by the apoptosis induction reagent. However, in SAS-Ly cells, the reagent induced no significant difference. Our findings indicate that the RAD21 gene was closely related to the invasion and metastasis of cancer cells.

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Section: Introductionmentioning

confidence: 99%

Correlation of invasion and metastasis of cancer cells, and expression of the RAD21 gene in oral squamous cell carcinoma

et al. 2006

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“…7). Endoreduplicated chromosomes are not observed, suggesting that even with an active spindle checkpoint, Cdk1 inactivation somehow leads to loss of chromosome cohesion, presumably by destruction of cohesins (Nasmyth et al 2000). Potapova et al (2006) have also shown that Cdk1 inhibition in mitotic cells leads to chromatid separation, provided that the proteasome is active.…”

Section: Discussionmentioning

confidence: 99%

Inactivation of Cdk1/Cyclin B in metaphase-arrested mouse FT210 cells induces exit from mitosis without chromosome segregation or cytokinesis and allows passage through another cell cycle

Paulson

2007

Chromosoma

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It is well known that inactivation of Cdk1/Cyclin B is required for cells to exit mitosis. The work reported here tests the hypothesis that Cdk1/Cyclin B inactivation is not only necessary but also sufficient to induce mitotic exit and reestablishment of the interphase state. This hypothesis predicts that inactivation of Cdk1 in metaphase-arrested cells will induce the M to G1-phase transition. It is shown that when mouse FT210 cells (in which Cdk1 is temperature-sensitive) are arrested in metaphase and then shifted to their non-permissive temperature, they rapidly exit mitosis as evidenced by reassembly of interphase nuclei, decondensation of chromosomes, and dephosphorylation of histones H1 and H3. The resulting interphase cells are functionally normal as judged by their ability to progress through another cell cycle. However, they have double the normal number of chromosomes because they previously bypassed anaphase, chromosome segregation, and cytokinesis. These results, taken together with other observations in the literature, strongly suggest that in mammalian cells, inactivation of Cdk1/cyclin B is the trigger for mitotic exit and reestablishment of the interphase state.

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“…DNA replication produces two identical sister chromatids which are held together by cohesin complexes [5]. The rule of strict alternation requires that DNA replication is followed by chromosome segregation (anaphase) which depends on removal of cohesins from chromosomes.…”

Section: Alternation Of Chromosome Replication and Segregationmentioning

confidence: 99%

“…Origin firing and licensing are co-ordinated via Cdk activity, which besides activating origin firing, also inactivates components in the licensing system [4]. Therefore replication origins are licensed in a low Cdk activity (G 1 ) phase of the cell cycle ( Figure 1).DNA replication produces two identical sister chromatids which are held together by cohesin complexes [5]. The rule of strict alternation requires that DNA replication is followed by chromosome segregation (anaphase) which depends on removal of cohesins from chromosomes.…”

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confidence: 99%

Systems-level feedback in cell-cycle control

Novák

Vinod

Freire

et al. 2010

Biochemical Society Transactions

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Alternation of chromosome replication and segregation is essential for successful completion of the cell cycle and it requires an oscillation of Cdk1 (cyclin-dependent kinase 1)-CycB (cyclin B) activity. In the present review, we illustrate the essential features of checkpoint controlled and uncontrolled cell-cycle oscillations by using mechanical metaphors. Despite variations in the molecular details of the oscillatory mechanism, the underlying network motifs responsible for the oscillations are always well-conserved. The checkpoint-controlled cell cycles are always driven by a negative-feedback loop amplified by double-negative feedbacks (antagonism).

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Splitting the Chromosome: Cutting the Ties that Bind Sister Chromatids

Cited by 38 publications

References 0 publications

Correlation of invasion and metastasis of cancer cells, and expression of the RAD21 gene in oral squamous cell carcinoma

Correlation of invasion and metastasis of cancer cells, and expression of the RAD21 gene in oral squamous cell carcinoma

Inactivation of Cdk1/Cyclin B in metaphase-arrested mouse FT210 cells induces exit from mitosis without chromosome segregation or cytokinesis and allows passage through another cell cycle

Systems-level feedback in cell-cycle control

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