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PubMed1983

C heterochromatin variation in couples with recurrent early abortions.

The possible influence of the high polymorphic C heterochromatic regions of human chromosomes 1, 9, 16, and Y on meiotic chromosome segregation was investigated. Faulty chromosome segregation may be the result of either an abnormal quantity of C heterochromatin on the homologues, or disequilibrium between the homologues. The aim of our study was to determine whether either a variation in the amounts of total C heterochromatin or differences in the amounts of C heterochromatin between homologues could lead to faulty chromosome segregation. The study was performed on C banded metaphases obtained from peripheral lymphocyte cultures of 15 couples with recurrent early abortions and 15 control couples, all Caucasians. Analysis of variance was first performed on separate metaphases to measure intra-individual, inter-individual, and between population variation in a hierarchical model. Since the significant intra-individual differences covered the other parameters we performed, secondly, a one way analysis of variance on the mean values of metaphases per person in order to measure the inter-individual and between population variation. The results did not show a relationship between C heterochromatin lengths and occurrence of recurrent abortions.

Abortion, Habitual↗
PubMed1996

Sex ratio in normal and disomic sperm: evidence that the extra chromosome 21 preferentially segregates with the Y chromosome.

In humans, deviations from a 1:1 male:female ratio have been identified in both chromosomally normal and trisomic live births: among normal newborns there is a slight excess of males, among trisomy 18 live borns a large excess of females, and among trisomy 21 live borns an excess of males. These differences could arise from differential production of or fertilization by Y- or X-bearing sperm or from selection against male or female conceptions. To examine the proportion of Y- and X-bearing sperm in normal sperm and in sperm disomic for chromosomes 18 or 21, we used three-color FISH (to the X and Y and either chromosome 18 or chromosome 21) to analyze >300,000 sperm from 24 men. In apparently normal sperm, the sex ratio was nearly 1:1 (148,074 Y-bearing to 148,657 X-bearing sperm), and the value was not affected by the age of the donor. Certain of the donors, however, had significant excesses of Y- or X-bearing sperm. In disomy 18 sperm, there were virtually identical numbers of Y- and X-bearing sperm; thus, the excess of females in trisomy 18 presumably is due to selection against male trisomic conceptions. In contrast, we observed 69 Y-bearing and 44 X-bearing sperm disomic for chromosome 21. This is consistent with previous molecular studies, which have identified an excess of males among paternally derived cases of trisomy 21, and suggests that some of the excess of males among Down syndrome individuals is attributable to a nondisjunctional mechanism in which the extra chromosome 21 preferentially segregates with the Y chromosome.

Chromosomes, Human, Pair 18↗
PubMed1977

Suppression of production of mouse 28S ribosomal RNA in mouse-human hybrids segregating mouse chromosomes.

Mouse-human somatic cell hybrids that lose (segregate) human chromosomes produce only mouse 28S ribosomal RNA even when they retain copies of the human chromosomes that contain the genes for 28S ribosomal RNA. In contrast, mouse-human hybrid cells that segregate mouse chromosomes produce only human 28S ribosomal RNA even when they have retained copies of mouse chromosomes that contain the 28S ribosomal RNA genes.

Animals↗
PubMed1988

Caffeine interactions with methyl methanesulphonate, hycanthone, benlate, and cadmium chloride in chromosomal meiotic segregation of Saccharomyces cerevisiae.

Interactions of caffeine with chemicals known for their effects on chromosomal segregation during meiosis of Saccharomyces cerevisiae were studied. It appears that caffeine does interfere with the action of other compounds during the different phases of meiosis. Treatments with methyl methanesulphonate (MMS) and cadmium chloride (CdCl2) resulted in a synergistic effect consisting of an increase in the frequency of recombination. The greatest effects were found on the induction of diploid spores: MMS, hycanthone, and distamycin demonstrated strong, benlate little synergistic action. CdCl2 demonstrated antagonism to caffeine by counter-inhibiting its effect on the induction of diploids. Concerning disomic induction: caffeine reduced (or left unchanged) the effect on non-disjunction when MMS and hycanthone were used. Simple additive effects were caused in conjunction with distamycin, benlate, and (in small doses) CdCl2. 2 mg of caffeine/ml in treatments with CdCl2 resulted in a very high frequency of disomic clones.

Benomyl↗
PubMed2004

Condensin restructures chromosomes in preparation for meiotic divisions.

The production of haploid gametes from diploid germ cells requires two rounds of meiotic chromosome segregation after one round of replication. Accurate meiotic chromosome segregation involves the remodeling of each pair of homologous chromosomes around the site of crossover into a highly condensed and ordered structure. We showed that condensin, the protein complex needed for mitotic chromosome compaction, restructures chromosomes during meiosis in Caenorhabditis elegans. In particular, condensin promotes both meiotic chromosome condensation after crossover recombination and the remodeling of sister chromatids. Condensin helps resolve cohesin-independent linkages between sister chromatids and alleviates recombination-independent linkages between homologues. The safeguarding of chromosome resolution by condensin permits chromosome segregation and is crucial for the formation of discrete, individualized bivalent chromosomes.

Adenosine Triphosphatases↗
PubMed2002

[Disruption of organization of mitotic microtubules in root meristem cells of Allium cepa induced by chloral hydrate].

Data are presented on the effect of chlorahydrate on microtubule organization in the root meristem of Allium cepa. Our studies show that an incomplete preprophase band commonly appears during G2-prophase transition, yet the major effect is the lack of perinuclear microtubules, leading to inhibition of the prophase spindle formation and transition to C-mitosis. Upon chloralhydrate treatment of metaphase cells, we found cells with chromosomes regularly aligned within the metaphase plate and differently disorganized mitotic spindles. Concurrently, C-metaphase cells with remnants of kinetochore fibers were present. In addition, normal bipolar and abnormal irregular types of chromosome segregation were detected, this representing multipolar and diffuse anaphases. The major difference between them is the presence of polar microtubules during multipolar anaphase, and their lacking during diffuse anaphase. Alternatively, microtubule clusters between segregated groups of chromosomes are typical for cells with diffuse anaphase. During bipolar anaphase, excessive aster-like microtubules emanate from the spindle poles, and in telophase accessory phragmoplasts are observed at the cell periphery. The formation of incomplete phragmoplasts was observed after normal bipolar and abnormal chromosome segregation. We conclude that chloralhydrate may affect the nuclear surface capability to initiate the growth of perinuclear microtubules, thus blocking the prophase spindle formation. It also disturbs the spatial interaction between microtubules, which is crucial for the formation and functioning of various microtubular systems (preprophase band, spindle and phragmoplast).

Allium↗
PubMed2006

Telomere dysfunction and loss of p53 cooperate in defective mitotic segregation of chromosomes in cancer cells.

Aneuploidy is a fundamental principle of many cancer cells and is mostly related to defects in mitotic segregation of chromosomes. Many solid tumors as well as some preneoplastic lesions have been shown to contain polyploid chromosome numbers. The exact mechanisms behind whole-genome duplications are not known but have been linked to compromised mitotic checkpoint genes. We now report that the telomere checkpoint plays a key role for polyploidy in colon cancer cells. Telomerase suppression by a dominant-negative mutant of hTERT and consecutive telomere dysfunction in wild-type HCT116 colon cancer cells resulted in only minor stable chromosomal alterations. However, higher ploidy levels with up to 350 chromosomes were found when the cell-cycle checkpoint proteins p53 or p21 were absent. These findings indicate that telomere dysfunction in the absence of cell-cycle control may explain the high frequency of alterations in chromosome numbers found in many solid tumors.

Chromosome Segregation↗
PubMed1998

Genetics of oocyte ageing.

OBJECTIVES: Correlations between parental age, aneuploidy in germ cells and recent findings on aetiological factors in mammalian trisomy formation are reviewed. METHODS: Data from observations in human oocytes, molecular studies on the origin of extra chromosomes in trisomies, experiments in a mouse model system, and transgenic approaches are shown. RESULTS: Errors in chromosome segregation are most frequent in meiosis I of oogenesis in mammals and predominantly predispose specific chromosomes and susceptible chiasmate configurations to maternal age-related nondisjunction. Studies on spindle structure, cell cycle and chromosome behaviour in oocytes of the CBA/Ca mouse used as a model for the maternal age-effect suggest that hormonal homeostasis and size of the follicle pool influence the quality, maturation competence and spindle size of the mammalian oocyte. Predisposition to errors in chromosome segregation are critically dependent on altered cell cycles. Compromised protein synthesis and mitochondrial function affect maturation kinetics and spindle formation, and cause untimely segregation of chromosomes (predivision), mimicking an aged phenotype. CONCLUSIONS: Altered cell cycles and untimely resolution of chiasmata but also nondisjunction of late segregating homologues caused by asynchrony in cytoplasmic and nuclear maturation appear to be causal to errors in chromosome segregation with advanced maternal age. Oocytes appear to lack checkpoints guarding against untimely chromosome segregation. Genes and exposures affecting pool size, hormonal homeostasis and interactions between oocytes and their somatic compartment and thus quality of follicles and oocytes have the potential to critically influence chromosome distribution in female meiosis and affect fertility in humans and other mammals.

Aging↗
PubMed2004

Structure and segregation of the bacterial nucleoid.

In bacteria, chromosome segregation and DNA replication occur concurrently and there is no clear equivalent of a eukaryote mitotic spindle. Chromosome segregation can be viewed as a two-step process. As the first step, the origin of replication regions are segregated actively, probably by a mechanism involving an as yet unidentified motor protein or proteins, and held in position. The second step is the separation and migration of the rest of the chromosome probably driven by forces generated from various cellular processes such as DNA replication, transcription and transertion.

Bacillus subtilis↗
PubMed1998

Sperm segregation analysis of a complex chromosome rearrangement, 2;22;11, by whole chromosome painting.

Using the human sperm-hamster oocyte fusion technique and whole chromosome painting, we studied sperm chromosome segregation in a male heterozygous for a complex chromosome rearrangement, 46,XY,-2, +der(2)t(2;11)(q13; q23),-11,+der(11)t(11;22)(q23;q11.2),-22, +der(22)t(2;22)(q13; q11.2). A total of 208 sperm complements were analyzed. The frequency of sperm carrying a normal or a balanced complement was 13.5% (9.62% and 3.85%, respectively). The frequency of unbalanced sperm was 86.5% (64.9% from 3:3 segregation, including 30 different types; 20.7% from 4:2 segregation, including 21 different types; and 0.96% from 5:1 segregation, including 2 different types). The sex ratio, determined in 134 sperm complements, did not differ from the expected 1:1 ratio. The results obtained in this study are compatible with the formation, during the synaptic process, of a complex hexavalent figure involving chromosomes 2, 11, and 22. The behavior and segregation of this complex figure would explain the high frequency (86.5%) of unbalanced complements observed in this carrier.

Animals↗
PubMed2001

Nonrandom segregation during meiosis: the unfairness of females.

Most geneticists assume that chromosome segregation during meiosis is Mendelian (i.e., each allele at each locus is represented equally in the gametes). The great majority of reports that discuss non-Mendelian transmission have focused on systems of gametic selection, such as the mouse t-haplotype and Segregation distorter in Drosophila, or on systems in which post-fertilization selection takes place. Because the segregation of chromosomes in such systems is Mendelian and unequal representation of alleles among offspring is achieved through gamete dysfunction or embryonic death, there is a common perception that true disturbances in the randomness of chromosome segregation are rare and of limited biological significance. In this review we summarize data on nonrandom segregation in a wide variety of genetic systems. Despite apparent differences between some systems, the basic requirements for nonrandom segregation can be deduced from their shared characteristics: i) asymmetrical meiotic division(s); ii) functional asymmetry of the meiotic spindle poles; and iii) functional heterozygosity at a locus that mediates attachment of a chromosome to the spindle. The frequency with which all three of these requirements are fulfilled in natural populations is unknown, but our analyses indicate that nonrandom segregation occurs with sufficient frequency during female meiosis, and in exceptional cases of male meiosis, that it has important biological, clinical, and evolutionary consequences.

Animals↗
PubMed1990

Mixed segregation of chromosomes during single-division meiosis of Saccharomyces cerevisiae.

Normal meiosis consists of two consecutive cell divisions in which all the chromosomes behave in a concerted manner. Yeast cells homozygous for the mutation cdc5, however, may be directed through a single meiotic division of a novel type. Dyad analysis of a cdc5/cdc5 strain with centromere-linked markers on four different chromosomes has shown that, in these meioses, some chromosomes within a given cell segregate reductionally whereas others segregate equationally. The choice between the two types of segregation in these meioses is made individually by each chromosome pair. Different chromosome pairs exhibit different segregation tendencies. Similar results were obtained for cells homozygous for cdc14.

Cell Division↗
PubMed1980

Marker segregation without chromosome loss at the emt locus in Chinese hamster cell hybrids.

Segregation, defined as the reexpression of the recessive phenotype, has been examined in Chinese hamster cell hybrids heterozygous at the recessive emtr locus. Segregants were selected in emetine, and the role of chromosome loss in the segregation process was evaluated by detailed karyotype comparison of segregants with their hybrid parent. In emtr CHO x emt+ CHO hybrids (CHO is thought to be hemizygous at the emt locus), segregants were obtained at high frequency, and no consistent chromosome loss was found in the segregants. In hybrids made with Emtr CHO and wild-type lines other than CHO (CHW,CHL,V-79), where two wild-type alleles are thought to be present in the hybrid, segregants were obtained at much lower frequency, consistent with a two-step segregation process. These segregants revealed consistent loss of one chromosome 2 or deletion of a part of the long arm of a chromosome 2. Thus, one step in segregation seems to be chromosome loss while the other step must have a different mechanism, possibly the same mechanism that operates in the CHO x CHO hybrids. Two major conclusions can be drawn: (1) the emt gene maps to a hemizygous region of the long arm of a chromosome 2 in Chinese hamster, and (2) a segregation mechanism other than chromosome loss appears to operate with high efficiency in intraspecific hybrids.

Aneuploidy↗
PubMed2002

Distinct functions of S. pombe Rec12 (Spo11) protein and Rec12-dependent crossover recombination (chiasmata) in meiosis I; and a requirement for Rec12 in meiosis II.

BACKGROUND: In most organisms proper reductional chromosome segregation during meiosis I is strongly correlated with the presence of crossover recombination structures (chiasmata); recombination deficient mutants lack crossovers and suffer meiosis I nondisjunction. We report that these functions are separable in the fission yeast Schizosaccharomyces pombe. RESULTS: Intron mapping and expression studies confirmed that Rec12 is a member of the Spo11/Top6A topoisomerase family required for the formation of meiotic dsDNA breaks and recombination. rec12-117, rec12-D15 (null), and rec12-Y98F (active site) mutants lacked most crossover recombination and chromosomes segregated abnormally to generate aneuploid meiotic products. Since S. pombe contains only three chromosome pairs, many of those aneuploid products were viable. The types of aberrant chromosome segregation were inferred from the inheritance patterns of centromere linked markers in diploid meiotic products. The rec12-117 and rec12-D15 mutants manifest segregation errors during both meiosis I and meiosis II. Remarkably, the rec12-Y98F (active site) mutant exhibited essentially normal meiosis I segregation patterns, but still exhibited meiosis II segregation errors. CONCLUSIONS: Rec12 is a 345 amino acid protein required for most crossover recombination and for chiasmatic segregation of chromosomes during meiosis I. Rec12 also participates in a backup distributive (achiasmatic) system of chromosome segregation during meiosis I. In addition, catalytically-active Rec12 mediates some signal that is required for faithful equational segregation of chromosomes during meiosis II.

Journal Article↗
PubMed1996

Chemical induction of mitotic checkpoint override in mammalian cells results in aneuploidy following a transient tetraploid state.

Populations of tetraploid cells are found in a variety of human tumours where they may act as precursors of aneuploidy and tumorigenesis. Here we demonstrate the drug induction of tetraploid cells at mitosis by interference with cell cycle checkpoints and the coordination of mitotic events. Tetraploid cells result from mitotic exit in the absence of either chromosome segregation or cytokinesis. One class of agents that induces tetraploidy causes override of cell cycle checkpoints that require metaphase chromosome alignment as a pre-condition for initiating exit from mitosis. As a result cells exposed to such drugs progress partially through mitosis, but exit without chromosome segregation or cytokinesis. Inhibitors of microtubule assembly comprise a second class of agents that induce tetraploidy. Many cell types are incapable of maintaining indefinite mitotic arrest in the presence of microtubule inhibitors and finally exit mitosis without microtubule dependent chromosome segregation. Inhibitors of topoisomerase II represent a third class of drugs that induce tetraploidy at mitosis. By inhibiting DNA decatenation required for sister chromatid separation at the onset of anaphase such drugs block chromosome segregation. When topoisomerase II activity is inhibited, cells nonetheless reform nuclei and exit from mitosis without chromosome segregation. Finally, inhibition of cleavage furrow formation by agents such as cytochalasins represents a fourth mechanism of tetraploidization at mitosis. We find that when Chinese Hamster Ovary cells become tetraploid, regardless of which mechanism induces this state, they are genetically unstable and become aneuploid at the subsequent mitosis. In conclusion, the failure of mitotic checkpoint function can generate gross aneuploidy from which cells with an advantage for tumor growth may be selected.

2-Aminopurine↗
PubMed1990

Analysis of a model for minichromosome segregation in Escherichia coli.

The present article contains a theoretical, quantitative analysis of the implications of the Helmstetter-Leonard model (1987, J. molec. Biol. 197, 195-204.) for the segregation of chromosomal DNA in Escherichia coli, on the expected copy-number distribution of minichromosomes in a culture in steady-state exponential growth. According to the model, two determinants are involved in the mechanism of chromosome segregation: a partition system that assures the equal allotment of chromosomes between daughter cells at cell division, and a locus within the minimal oriC region that specifies the attachment site of the chromosomes to the cell envelope at initiation of replication. There are many parameters that must be taken into account in such a study, and since some of them are probabilistic in nature, a strictly analytical approach is not feasible and we had to resort to computer simulation. A wide range of parameter values was tested, in all combinations. The minichromosome copy-number distributions obtained all had a prominent mode equal to the number of oriC binding sites and their main features were determined essentially by that and very little by any of the other parameters of the model. In order to avoid the unrealistic situation in which this one feature completely dominates the results, the original model was modified so that each individual minichromosome is no longer required to replicate during every cell generation, by introducing a limit to the number of unsuccessful attempts to locate a suitable binding site. The copy-number distributions predicted by this version of the model are quantitatively and qualitatively very different and depend on all the components of the model. The simulation results are sufficiently well-behaved to allow consideration as to whether a particular empirical minichromosome copy-number distribution--when such data become available--could in fact be governed by the proposed model; it may even be possible to get a rough estimate for the different parameters involved.

Computer Simulation↗
PubMed2004

A Role for the RSC chromatin remodeler in regulating cohesion of sister chromatid arms.

The precise segregation of chromosomes is critical for the proliferation and development of living organisms. Defects in this process can result in tumorigenesis and hereditary diseases. The four-subunit cohesin complex plays an essential role in chromosome segregation and genome integrity. Recently, we reported that the association of cohesin with centromeres and chromosome arms is differentially regulated by the ATP-dependent RSC chromatin-remodeling complex. Here, we propose two models to explain why the cell should have evolved special mechanisms for centromeric and sister arm cohesion and why RSC differentially regulates these processes.

Animals↗
PubMed2003

Actin-like proteins MreB and Mbl from Bacillus subtilis are required for bipolar positioning of replication origins.

Actin-like proteins MreB and Mbl are required for proper cell shape and for viability in B. subtilis and form dynamic helical filaments underneath the cell membrane. We have found that depletion of MreB and Mbl proteins leads to a rapid defect in chromosome segregation before a defect in cell shape becomes detectable. Under these conditions, the SMC chromosome segregation complex that is essential for proper chromosome arrangement and segregation loses its specific subcellular localization, and replication origins fail to localize in a regular bipolar manner as in wild type cells. Time-lapse microscopy showed that during depletion of MreB, origin regions can move towards the same cell pole, showing that bipolar orientation of origin separation is lost. Contrarily, depletion of three other cell shape determinants, MreC, MreD, or MreBH (the third B. subtilis actin homolog) had no effect on chromosome segregation but varying effects on cell morphology. Depletion of MreC and MreD resulted in formation of round cells, while depletion of MreBH led to formation of vibrio-shaped cells. The data show that actin proteins Mbl and MreB are required for proper chromosome segregation and that Mre proteins affect different aspects in cell shape.

Actins↗