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PubMed2006

Chromosome segregation in fission yeast with mutations in the tubulin folding cofactor D.

Faithful chromosome segregation requires the combined activities of the microtubule-based mitotic spindle and the multiple proteins that form mitotic kinetochores. Here, we show that the fission yeast mitotic mutant, tsm1-512, is an allele of the tubulin folding chaperone, cofactor D. Chromosome segregation in this and in an additional cofactor D mutant depends on growth conditions that are monitored specifically by the mitotic checkpoint proteins Mad1, 2, 3 and Bub3. The temperature-sensitive mutants we have used disrupt the function of cofactor D to different extents, but both strains form a mitotic spindle in which the poles separate in anaphase. However, chromosome segregation is often unequal, apparently due to a defect in kinetochore-microtubule interactions. Mutations in cofactor D render cells particularly sensitive to the expression levels of a CENP-B-like protein, Abp1p, which works as an allele-specific, high-copy suppressor of cofactor D. This and other genetic interactions between cofactor D mutants and specific kinetochore and spindle components suggest their critical role in establishing the normal kinetochore-microtubule interface.

Alleles↗

PubMed1985

Chromosome segregation and spindle structure in crane fly spermatocytes following Colcemid treatment.

Chromosome segregation in primary spermatocytes of the crane fly Nephrotoma suturalis was studied after exposure to Colcemid at doses that did not completely inhibit spindle formation. Colcemid was added either to the medium in which larvae were cultured or to Tricine buffer in which isolated testes were incubated. Patterns of chromosome segregation were analyzed in fixed, Feulgen-stained smears of testes from Colcemid-treated larvae and in living cell preparations. Anomalies observed during the first meiotic division at higher than normal frequencies in Colcemid-treated spermatocytes included anaphase lagging of autosomes, chromosomal strands, tripolar and tetrapolar divisions, and unequal distribution of chromosomes to secondary cells. Following those doses of Colcemid that induced the above anomalies, the length of the birefringent spindle in primary spermatocytes was shorter than normal. This effect on spindle length also was apparent in Giemsa-stained preparations of fixed cells, in which the two centrosomes at the spindle poles were differentiated from the rest of the cytoplasm. The results indicate a correlation between the inhibition of spindle formation and the induction of anomalous patterns of chromosome segregation.

Animals↗

PubMed1999

Chromosome segregation during the prokaryotic cell division cycle.

Recent work has dramatically changed our view of chromosome segregation in bacteria. Rather than being a passive process, it involves rapid movement of parts of the circular chromosome. Several genes involved in chromosome segregation have been identified, and the analysis of their functions and intracellular localization are beginning to shed light on the mechanisms that ensure efficient chromosome segregation.

Bacillus subtilis↗

PubMed2005

The CNA1 histone of the ciliate Tetrahymena thermophila is essential for chromosome segregation in the germline micronucleus.

Ciliated protozoans present several features of chromosome segregation that are unique among eukaryotes, including their maintenance of two nuclei: a germline micronucleus, which undergoes conventional mitosis and meiosis, and a somatic macronucleus that divides by an amitotic process. To study ciliate chromosome segregation, we have identified the centromeric histone gene in the Tetrahymena thermophila genome (CNA1). CNA1p specifically localizes to peripheral centromeres in the micronucleus but is absent in the macronucleus during vegetative growth. During meiotic prophase of the micronucleus, when chromosomes are stretched to twice the length of the cell, CNA1p is found localized in punctate spots throughout the length of the chromosomes. As conjugation proceeds, CNA1p appears initially diffuse, but quickly reverts to discrete dots in those nuclei destined to become micronuclei, whereas it remains diffuse and is gradually lost in developing macronuclei. In progeny of germline CNA1 knockouts, we see no defects in macronuclear division or viability of the progeny cells immediately following the knockout. However, within a few divisions, progeny show abnormal mitotic segregation of their micronucleus, with most cells eventually losing their micronucleus entirely. This study reveals a strong dependence of the germline micronucleus on centromeric histones for proper chromosome segregation.

Animals↗

PubMed2006

Actin homolog MreB and RNA polymerase interact and are both required for chromosome segregation in Escherichia coli.

The actin-like MreB cytoskeletal protein and RNA polymerase (RNAP) have both been suggested to provide the force for chromosome segregation. Here, we identify MreB and RNAP as in vivo interaction partners. The interaction was confirmed using in vitro purified components. We also present convincing evidence that MreB and RNAP are both required for chromosome segregation in Escherichia coli. MreB is required for origin and bulk DNA segregation, whereas RNAP is required for bulk DNA, terminus, and possibly also for origin segregation. Furthermore, flow cytometric analyses show that MreB depletion and inactivation of RNAP confer virtually identical and highly unusual chromosome segregation defects. Thus, our results raise the possibility that the MreB-RNAP interaction is functionally important for chromosome segregation.

Actins↗

PubMed2004

The occurrence of chromosome segregational defects is an intrinsic and heritable property of oral squamous cell carcinoma cell lines.

Chromosomal segregational defects are commonly observed in cancer cells and are an important source of genetic instability. It is currently unknown whether these mitotic defects are the result of a subpopulation of defective cells or reflect characteristics of the population of cells as a whole. In this study, we compared chromosomal segregational defects in two oral squamous cell carcinoma cell lines and five single-cell clones from each of those cell lines. We used immunofluorescence microscopy to quantitate the occurrence of multipolar metaphase spindles, lagging chromosomes at metaphase and anaphase, and anaphase bridges. We conclude that chromosome segregational defects in these cancer cell lines represent an intrinsic and inherited tendency toward segregational defects in the general cell population, rather than the existence of a subpopulation of cells with segregational defects.

Carcinoma, Squamous Cell↗

PubMed2004

"Holo"er than thou: chromosome segregation and kinetochore function in C. elegans.

Kinetochores are proteinaceous organelles that assemble on centromeric DNA to direct chromosome segregation in all eukaryotes. While many aspects of kinetochore function are conserved, the nature of the chromosomal domain upon which kinetochores assemble varies dramatically between different species. In monocentric eukaryotes, kinetochores assemble on a localized region of each chromosome. In contrast, holocentric species such as the nematode Caenorhabditis elegans have diffuse kinetochores that form along the entire length of their chromosomes. Here, we discuss the nature of chromosome segregation in C. elegans. In addition to reviewing what is known about kinetochore function, chromosome structure, and chromosome movement, we consider the consequences of the specialized holocentric architecture on chromosome segregation.

Animals↗

PubMed2003

Chromosome segregation: clamping down on deviant orientations.

Chromosome segregation depends on proper orientation of sister kinetochores. The protein Csm1 is required for mono-orientation of sister kinetochores at meiosis I in budding yeast. Surprisingly, its homologue in fission yeast appears instead of clamp micro-tubule binding sites together on single mitotic kinetochores so that they all face one spindle pole.

Cell Cycle Proteins↗

PubMed2002

Bacterial chromosome segregation.

Recent studies have made great strides toward our understanding of the mechanisms of microbial chromosome segregation and partitioning. This review first describes the mechanisms that function to segregate newly replicated chromosomes, generating daughter molecules that are viable substrates for partitioning. Then experiments that address the mechanisms of bulk chromosome movement are summarized. Recent evidence indicates that a stationary DNA replication factory may be responsible for supplying the force necessary to move newly duplicated DNA toward the cell poles. Some factors contributing to the directionality of chromosome movement probably include centromere-like-binding proteins, DNA condensation proteins, and DNA translocation proteins.

Bacterial Proteins↗

PubMed2002

The 2 micron plasmid purloins the yeast cohesin complex: a mechanism for coupling plasmid partitioning and chromosome segregation?

The yeast 2 micron plasmid achieves high fidelity segregation by coupling its partitioning pathway to that of the chromosomes. Mutations affecting distinct steps of chromosome segregation cause the plasmid to missegregate in tandem with the chromosomes. In the absence of the plasmid stability system, consisting of the Rep1 and Rep2 proteins and the STB DNA, plasmid and chromosome segregations are uncoupled. The Rep proteins, acting in concert, recruit the yeast cohesin complex to the STB locus. The periodicity of cohesin association and dissociation is nearly identical for the plasmid and the chromosomes. The timely disassembly of cohesin is a prerequisite for plasmid segregation. Cohesin-mediated pairing and unpairing likely provides a counting mechanism for evenly partitioning plasmids either in association with or independently of the chromosomes.

Bacterial Proteins↗

PubMed2003

mSin3-associated protein, mSds3, is essential for pericentric heterochromatin formation and chromosome segregation in mammalian cells.

The histone code guides many aspects of chromosome biology including the equal distribution of chromosomes during cell division. In the chromatin domains surrounding the centromere, known as pericentric heterochromatin, histone modifications, particularly deacetylation and methylation, appear to be essential for proper chromosome segregation. However, the specific factors and their precise roles in this highly orchestrated process remain under active investigation. Here, we report that germ-line or somatic deletion of mSds3, an essential component of the functional mSin3/HDAC corepressor complex, generates a cell-lethal condition associated with rampant aneuploidy, defective karyokinesis, and consequently, a failure of cytokinesis. mSds3-deficient cells fail to deacetylate and methylate pericentric heterochromatin histones and to recruit essential heterochromatin-associated proteins, resulting in aberrant associations among heterologous chromosomes via centromeric regions and consequent failure to properly segregate chromosomes. Mutant mSds3 molecules that are defective in mSin3 binding fail to rescue the mSds3 null phenotypes. On the basis of these findings, we propose that mSds3 and its associated mSin3/HDAC components play a central role in initiating the cascade of pericentric heterochromatin-specific modifications necessary for the proper distribution of chromosomes during cell division in mammalian cells.

Acetylation↗

PubMed2005

A cis-acting sequence involved in chromosome segregation in Escherichia coli.

Eukaryotic chromosomes contain a locus, the centromere, at which force is applied to separate replicated chromosomes. A centromere analogue is also found in some bacterial plasmids and chromosomes, although not yet identified in the well-studied Escherichia coli chromosome. We aimed to identify centromere-like sequences in E. coli with the premise that such sequences would be the first to migrate towards the cell poles, away from the cell centre where DNA replication is believed to occur. We have labelled different loci on the chromosome by integrating arrays of binding sites for LacI-EYFP and phage lambdacI-ECFP and supplying these fusion proteins in trans. Comparison of such pairs of loci suggests the presence of a centromere-like site close to the origin of replication. Polar migration of the site was dependent on migS, a locus recently implicated in chromosome migration, thus providing strong support for migS being the E. coli centromere.

Base Sequence↗

PubMed1989

The claret locus in Drosophila encodes products required for eyecolor and for meiotic chromosome segregation.

The claret (ca) locus in Drosophila encodes products that are needed both for wild-type eyecolor and for correct meiotic chromosome segregation. Mutants described previously provide evidence that two mutationally independent coding regions are present at ca. We have recovered six new P element-induced and one spontaneous ca mutant. Four of these new mutants affect both eyecolor and chromosome segregation. The high frequency of co-mutation of these two functions suggests that the corresponding genes are closely adjacent to one another. We recovered genomic DNA sequences corresponding to the ca locus by chromosome walking, and showed using revertant analysis that the cloned region encodes ca+. Transformation experiments demonstrate that the mutant effect resulting in meiotic chromosome non-disjunction (nd) and loss is fully rescued by DNA from the cloned region. Two RNAs of 7.4 and 2.2 kb have been identified by Northern blot analysis as the putative eyecolor and segregational products. Expression of the RNAs with respect to males and females, and their presence or absence in ca and nd mutants indicate that the 7.4 kb RNA corresponds to the product needed for wild-type eyecolor and the 2.2 kb RNA is the product required for normal chromosome segregation. These RNAs are transcribed in opposite directions to one another. Alleles that affect both eyecolor and chromosome segregation are deletion mutants that affect both transcripts. Thus, the putative eyecolor and segregational products are encoded by separate genes. Mutants that affect both eyecolor and chromosome segregation apparently do so because they delete essential regions of both genes.

Alleles↗

PubMed1999

The Aurora/Ipl1p kinase family: regulators of chromosome segregation and cytokinesis.

Members of the Aurora/Ipl1p family of mitotically regulated serine/threonine kinases are emerging as key regulators of chromosome segregation and cytokinesis. Proper chromosome segregation and cytokinesis ensure that each daughter cell receives the full complement of genetic material. Defects in these processes can lead to aneuploidy and the propagation of genetic abnormalities. This review discusses the Aurora/Ipl1p kinases in terms of their protein structure and proposed function in mitotic cells and also the potential role of aurora2 in human cancer.

Animals↗

PubMed2001

Chromosome segregation.

The ability to visualise specific genes and proteins within bacterial cells is revolutionising knowledge of chromosome segregation. The essential elements appear to be the driving force behind DNA replication, which occurs at fixed cellular positions, the condensation of newly replicated DNA by a chromosome condensation machine located at the cell 1/4 and 3/4 positions, and molecular machines that act at midcell to allow chromosome separation after replication and movement of the sister chromosomes away from the division septum prior to cell division. This review attempts to provide a perspective on current views of the bacterial chromosome segregation mechanism and how it relates to other cellular processes.

Bacteria↗

PubMed1999

Cohesin Rec8 is required for reductional chromosome segregation at meiosis.

When cells exit from mitotic cell division, their sister chromatids lose cohesion and separate to opposite poles of the dividing cell, resulting in equational chromosome segregation. In contrast, the reductional segregation of the first stage of meiotic cell division (meiosis I) requires that sister chromatids remain associated through their centromeres and move together to the same pole. Centromeric cohesion is lost as cells exit from meiosis II and sister chromatids can then separate. The fission yeast cohesin protein Rec8 is specific to and required for meiosis. Here we show that Rec8 appears in the centromeres and adjacent chromosome arms during the pre-meiotic S phase. Centromeric Rec8 persists throughout meiosis I and disappears at anaphase of meiosis II. When the rec8 gene is deleted, sister chromatids separate at meiosis I, resulting in equational rather than reductional chromosome segregation. We propose that the persistence of Rec8 at centromeres during meiosis I maintains sister-chromatid cohesion, and that its presence in the centromere-adjacent regions orients the kinetochores so that sister chromatids move to the same pole. This results in the reductional pattern of chromosome segregation necessary to reduce a diploid zygote to haploid gametes.

Cell Cycle Proteins↗

PubMed2000

FtsK functions in the processing of a Holliday junction intermediate during bacterial chromosome segregation.

In bacteria with circular chromosomes, homologous recombination can generate chromosome dimers that cannot be segregated to daughter cells at cell division. Xer site-specific recombination at dif, a 28-bp site located in the replication terminus region of the chromosome, converts dimers to monomers through the sequential action of the XerC and XerD recombinases. Chromosome dimer resolution requires that dif is positioned correctly in the chromosome, and the activity of FtsK, a septum-located protein that coordinates cell division with chromosome segregation. Here, we show that cycles of XerC-mediated strand exchanges form and resolve Holliday junction intermediates back to substrate irrespective of whether conditions support a complete recombination reaction. The C-terminal domain of FtsK is sufficient to activate the exchange of the second pair of strands by XerD, allowing both intra- and intermolecular recombination reactions to go to completion. Proper positioning of dif in the chromosome and of FtsK at the septum is required to sense the multimeric state of newly replicated chromosomes and restrict complete Xer reactions to dimeric chromosomes.

Chromosome Segregation↗

PubMed2001

Pre-meiotic S phase is linked to reductional chromosome segregation and recombination.

Meiosis is initiated from G1 of the cell cycle and is characterized by a pre-meiotic S phase followed by two successive nuclear divisions. The first of these, meiosis I, differs from mitosis in having a reductional pattern of chromosome segregation. Here we show that meiosis can be initiated from G2 in fission yeast cells by ectopically activating the meiosis-inducing network. The subsequent meiosis I occurs without a pre-meiotic S phase and with decreased recombination, and exhibits a mitotic pattern of equational chromosome segregation. The subsequent meiosis II results in random chromosome segregation. This behaviour is similar to that observed in cells lacking the meiotic cohesin Rec8 (refs 3, 4), which becomes associated with chromosomes at G1/S phase, including the inner centromere, a region that is probably critical for sister-centromere orientation. If the expression of Rec8 is delayed to S phase/G2, then the centromeres behave equationally. We propose that the presence of Rec8 in chromatin is required at the pre-meiotic S phase to construct centromeres that behave reductionally and chromosome arms capable of a high level of recombination, and that this explains why meiosis is initiated from G1 of the cell cycle.

Chromosome Segregation↗