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PubMed1963

Inhibition of protein syntheses during meiosis and its bearing on intracellular regulation.

Several parameters of meiosis have been studied in cultured anthers of Trillium erectum. The accessibility of labeled substrates to meiotic cells and the fate of these substrates in relation to meiotic stage have been determined. Evidence has been adduced for the synthesis of RNA and protein during the meiotic cycle well after chromosome duplication. The effect of interfering with systems directly or indirectly connected with protein formation has been studied by means of chloramphenicol, 8-azaguanine, 5-methyltryptophan, and ethionine. Administration of these reagents at different intervals in the cycle elicits correspondingly different responses thereby indicating a periodicity in the activities of different systems. The following processes have been shown to be affected in these experiments: chromosome segregation, chromosome morphology, cytokinesis, wall synthesis, and enzyme appearance. The possibility of experimentally altering the normal sequence of events has also been shown.

Azaguanine↗
PubMed1990

Segregation of recombined chromosomes in meiosis I requires DNA topoisomerase II.

To understand better the similarities and differences between meiosis and mitosis, we examined the meiotic role of DNA topoisomerase II, an enzyme that is required mitotically to disentangle sister chromatids at the time of chromosome segregation. In meiosis, we found that topoisomerase II is required only at the time of nuclear division. When cold-sensitive top2 mutants are induced to sporulate at the restrictive temperature, they undergo premeiotic DNA synthesis and commitment to meiotic levels of recombination but fail to complete the first meiotic nuclear division. The introduction of a mutation blocking recombination relieves the requirement for topoisomerase II in meiosis I. These results suggest that topoisomerase II is required at the time of chromosome segregation in meiosis I for the resolution of recombined chromosomes.

Cell Nucleus↗
PubMedDate not supplied

[Visible and "cryptic" segregation of parental chromosomes in embryonic stem hybrid cells].

Chromosome segregation of the parental chromosomes was studied in 20 interspecific hybrid clones obtained by fusion of Mus musculus embryonic stem cells with Mus caroli splenocytes. FISH analysis with labeled species specific probes and microsatellite markers was used for identification of the parental chromosomes. Cytogenetic analysis has shown significant intra- and interclonal variability in chromosome numbers and ratios of the parental chromosomes in the hybrid cells: six clones contained all M. caroli chromosomes, nine clones showed moderate segregation of M. caroli chromosomes (from 1 to 7), and five clones showed extensive loss of M. caroli chromosomes (from 12 to complete loss of all M. caroli autosomes). Both methods demonstrated "cryptic" segregation of the somatic partner chromosomes. For instance, five clones with near-tetraploid chromosome sets contained only few M. caroli chromosomes (from 1 to 8). The data obtained suggest that the tetraploid chromosome set per se is not a sufficient criterion for conclusion on the absence of chromosome loss in the hybrid cells. Note that "cryptic" chromosome segregation occurred at a high frequency in the examined hybrid clones. Thus, "cryptic" segregation should be borne in mind for assessing pluripotency and genome reprogramming of embryonic stem hybrid cells.

Animals↗
PubMed2005

Barrier-to-autointegration factor is required to segregate and enclose chromosomes within the nuclear envelope and assemble the nuclear lamina.

Barrier-to-autointegration factor (BAF) binds dsDNA, LEM-domain proteins, and lamins. Caenorhabditis elegans BAF requires Ce-lamin and two LEM-domain proteins (Ce-emerin and Ce-MAN1) to localize during nuclear assembly. It was unknown whether Ce-lamin and LEM proteins, in turn, depend on Ce-BAF (mutually dependent structural roles). RNA interference-mediated down-regulation of Ce-BAF caused gross defects in chromosome segregation, chromatin decondensation, and mitotic progression as early as the two-cell stage, and embryos died at the approximately 100-cell stage. Nuclear pores reassembled, whereas Ce-lamin, Ce-emerin, and Ce-MAN1 bound chromatin but remained patchy and disorganized. The nuclear membranes formed but failed to enclose anaphase-bridged chromatin. Time-lapse imaging showed two phenotypes: anaphase-bridged chromatin that eventually resolved, and segregated chromatin that returned to the midzone. Thus, the assembly of BAF, lamins, and LEM-domain proteins is mutually dependent, and is required to capture segregated chromosomes within the nascent nuclear envelope. Embryos that escaped lethality by down-regulation of Ce-BAF grew into sterile adults with misplaced distal tip cells and gonads, further suggesting that mild postembryonic reductions in BAF disrupt tissue-specific functions.

Amino Acid Sequence↗
PubMed2005

SMC5 and SMC6 genes are required for the segregation of repetitive chromosome regions.

Structure chromosome (SMC) proteins organize the core of cohesin, condensin and Smc5-Smc6 complexes. The Smc5-Smc6 complex is required for DNA repair, as well as having another essential but enigmatic function. Here, we generated conditional mutants of SMC5 and SMC6 in budding yeast, in which the essential function was affected. We show that mutant smc5-6 and smc6-9 cells undergo an aberrant mitosis in which chromosome segregation of repetitive regions is impaired; this leads to DNA damage and RAD9-dependent activation of the Rad53 protein kinase. Consistent with a requirement for the segregation of repetitive regions, Smc5 and Smc6 proteins are enriched at ribosomal DNA (rDNA) and at some telomeres. We show that, following Smc5-Smc6 inactivation, metaphase-arrested cells show increased levels of X-shaped DNA (Holliday junctions) at the rDNA locus. Furthermore, deletion of RAD52 partially suppresses the temperature sensitivity of smc5-6 and smc6-9 mutants. We also present evidence showing that the rDNA segregation defects of smc5/smc6 mutants are mechanistically different from those previously observed for condensin mutants. These results point towards a role for the Smc5-Smc6 complex in preventing the formation of sister chromatid junctions, thereby ensuring the correct partitioning of chromosomes during anaphase.

Cell Cycle Proteins↗
PubMed1993

Mitotic spindle pole separation.

Eukaryotic cells utilize a microtubular spindle to segregate chromosomes during mitosis. Chromosome segregation requires the timely separation of the mitotic spindle poles to which the chromosomes are attached. Recent studies at the molecular and cellular levels have provided new insights into the mechanism and regulation of this process. On the one hand, the process now seems more complex, as redundant mechanisms apparently overlap in function during cell division. On the other hand, some of these processes may be acting continuously during the various stages of spindle pole separation, suggesting an underlying simplicity.

Journal Article↗
PubMed1989

The great GATC: DNA methylation in E. coli.

In Escherichia coli the methylation of the adenine in the sequence 5'-GATC-3' is catalysed by the dam gene product, a DNA adenine methylase. We review the proposed roles for this methylation, and the sequence it modifies, in mismatch repair, DNA-protein interaction, gene expression, the initiation of chromosome replication, chromosome segregation, chromosome structure and the occurrence of mutational hotspots.

Base Sequence↗
PubMed1987

Increased tumorigenicity of polyploid Ehrlich variants during growth in vivo is associated with karyotypic changes.

In previous studies, treatment of Ehrlich ascites tumors (EAT) with either Sendai virus, Herpes virus or neuraminidase produced variants that differed significantly from EAT in both tumorigenicity and karyotype. In this study, less tumorigenicity variants of EAT were isolated by culturing in media containing low concentrations of serum or without serum. In contrast to the relative stability of tumorigenicity in such variants cultured in vivo, the tumorigenicity of these variant clones passaged in vivo was variable, depending on the variant clone. During growth in vivo, 3 variant clones independently isolated from serum-free medium, low serum-containing medium and after neuraminidase treatment produced markedly heterogeneous tumors, and after 4 passages the tumors were about 1000 times more tumorigenic than the initial variants. In generating new tumors, the tumors always segregated chromosomes. The banded chromosome analysis of a variant clone isolated from serum-free medium and its malignant tumor showed that most of the chromosomes segregated from the clone were normal types. On the other hand, the tumorigenicity of Herpes virus-induced variants was unchanged during growth in vivo.

Animals↗
PubMed1997

Condensins, chromosome condensation protein complexes containing XCAP-C, XCAP-E and a Xenopus homolog of the Drosophila Barren protein.

We report here purification and characterization of chromosome condensation protein complexes (termed condensins) containing XCAP-C and XCAP-E, two Xenopus members of the SMC family. Sucrose density gradient centrifugation reveals two major forms of condensins. The 8S form is a heterodimer of XCAP-C and XCAP-E, whereas the 13S form contains three additional subunits. One of them is identified as a homolog of the Drosophila Barren protein whose mutation shows a defect in chromosome segregation. Chromosomal targeting of condensins is mitosis-specific and is independent of topoisomerase IIalpha. 13S condensin is required for condensation, as demonstrated by immunodepletion and rescue experiments. Our results suggest that the condensin complexes represent the most abundant structural components of mitotic chromosomes and play a central role in driving chromosome condensation.

Adenosine Triphosphatases↗
PubMed2000

Centrosomes: Sic transit gloria centri.

Centrosomes are thought to ensure spindle bipolarity and thus correct chromosome segregation during mitosis, but recent studies indicate that somatic cells have an alternative mechanism that enables them to form a bipolar spindle and segregate chromosomes independently of centrosomes.

Centrosome↗
PubMed2000

Microtubules, membranes and cytokinesis.

Proper division of the cell requires coordination between chromosome segregation by the mitotic spindle and cleavage of the cell by the cytokinetic apparatus. Interactions between the mitotic spindle, the contractile ring and the plasma membrane ensure that the cleavage furrow is properly placed between the segregating chromosomes and that new membrane compartments are formed to produce two daughter cells. The microtubule midzone is able to stimulate the cortex of the cell to ensure proper ingression and completion of the cleavage furrow. Specialized microtubule structures are responsible for directing membrane vesicles to the site of cell cleavage, and vesicle fusion is required for the proper completion of cytokinesis.

Animals↗
PubMed1999

The top3(+) gene is essential in Schizosaccharomyces pombe and the lethality associated with its loss is caused by Rad12 helicase activity.

The topoisomerase III gene ( top3 (+)) from Schizosaccharomyces pombe was isolated and a targeted gene disruption ( top3 :: kan (R)) was used to make a diploid strain heterozygous for top3 (+). The diploid was sporulated and the top3 :: kan (R)spores went through four to eight cell divisions before arresting as elongated, predominantly binucleated cells with incompletely segregated chromosomes. This demonstrates that top3 (+)is essential for vegetative growth in fission yeast. The aberrant chromosomal segregation seen in top3 :: kan (R)cells is unlike the 'cut' phenotype seen in mitosis-defective mutants and so we refer to this phenotype as 'torn'. A deletion mutant, rad12-hd ( rad12 is a homolog of Saccharomyces cerevisiae SGS1), partially suppressed the lethality of top3 mutants. A point mutant, rad12-K547I, which presumably eliminates helicase activity, also suppresses the lethality of top3 mutants, demonstrating that the lethality seen in top3 (-)cells is most likely caused by the helicase activity of Rad12. This double mutant grows very slowly and has much lower viability compared to rad12-hd top3 :: kan (R)cells, implying that the helicase activity of Rad12 is not the only cause of top3 (-)lethality. The low viability of rad12 (-) top3 (-)mutants compared with rad12 single mutants suggests that Top3 also functions independently of Rad12.

Amino Acid Sequence↗
PubMed2005

The roles of MAD1, MAD2 and MAD3 in meiotic progression and the segregation of nonexchange chromosomes.

Errors in meiotic chromosome segregation are the leading cause of spontaneous abortions and birth defects. In humans, chromosomes that fail to experience crossovers (or exchanges) are error-prone, more likely than exchange chromosomes to mis-segregate in meiosis. We used a yeast model to investigate the mechanisms that partition nonexchange chromosomes. These studies showed that the spindle checkpoint genes MAD1, MAD2 and MAD3 have different roles. We identified a new meiotic role for MAD3; though dispensable for the segregation of exchange chromosomes, it is essential for the segregation of nonexchange chromosomes. This function of Mad3p could also be carried out by human BubR1. MAD1 and MAD2 act in a surveillance mechanism that mediates a metaphase delay in response to nonexchange chromosomes, whereas MAD3 acts as a crucial meiotic timer, mediating a prophase delay in every meiosis. These findings suggest plausible models for the basis of errant meiotic segregation in humans.

Cell Cycle Proteins↗
PubMed2005

Unequal segregation of parental chromosomes in embryonic stem cell hybrids.

Chromosome segregation was studied in 14 intra- and 20 inter-specific hybrid clones generated by fusion of Mus musculus embryonic stem (ES) cells with fibroblasts or splenocytes of DD/c mice or Mus caroli. As a control for in vitro evolution of tetraploid karyotype we used a set of hybrid clones obtained by fusion of ES cells (D3) with ES cells (TgTP6.3). Identification of the parental chromosomes in the clones was performed by microsatellite analysis and in situ hybridization with labeled species-specific probes. Both analyses have revealed three types of clones: (i) stable tetraploid, observed only for ES x ES cell hybrids; (ii) bilateral loss of chromosomes of both ES and somatic partners; (iii) unilateral segregation of chromosomes of the somatic partner. Observed unilateral segregation was extensive in ES-splenocyte cell hybrids, but lower in ES-fibroblast hybrid clones. Developmental state of the somatic partner is presumably responsible for directional chromosome loss. Nonrandom segregation implies that initial differences in the parental homologous chromosomes were not immediately equalized implying at least transient persistence of the differentiated epigenotype.

Animals↗
PubMed2005

SMC complexes in bacterial chromosome condensation and segregation.

Bacterial chromosomes segregate via a partition apparatus that employs a score of specialized proteins. The SMC complexes play a crucial role in the chromosome partitioning process by organizing bacterial chromosomes through their ATP-dependent chromatin-compacting activity. Recent progress in the composition of these complexes and elucidation of their structural and enzymatic properties has advanced our comprehension of chromosome condensation and segregation mechanics in bacteria.

Amino Acid Sequence↗
PubMed2004

Human chromokinesin KIF4A functions in chromosome condensation and segregation.

Accurate chromosome alignment at metaphase and subsequent segregation of condensed chromosomes is a complex process involving elaborate and only partially characterized molecular machinery. Although several spindle associated molecular motors have been shown to be essential for mitotic function, only a few chromosome arm--associated motors have been described. Here, we show that human chromokinesin human HKIF4A (HKIF4A) is an essential chromosome-associated molecular motor involved in faithful chromosome segregation. HKIF4A localizes in the nucleoplasm during interphase and on condensed chromosome arms during mitosis. It accumulates in the mid-zone from late anaphase and localizes to the cytokinetic ring during cytokinesis. RNA interference--mediated depletion of HKIF4A in human cells results in defective prometaphase organization, chromosome mis-alignment at metaphase, spindle defects, and chromosome mis-segregation. HKIF4A interacts with the condensin I and II complexes and HKIF4A depletion results in chromosome hypercondensation, suggesting that HKIF4A is required for maintaining normal chromosome architecture. Our results provide functional evidence that human KIF4A is a novel component of the chromosome condensation and segregation machinery functioning in multiple steps of mitotic division.

Adenosine Triphosphatases↗
PubMed2000

Non-Mendelian segregation of sex chromosomes in heterospecific Drosophila males.

Interspecific hybrids and backcrossed organisms generally suffer from reduced viability and/or fertility. To identify and genetically map these defects, we introgressed regions of the Drosophila sechellia genome into the D. simulans genome. A female-biased sex ratio was observed in 24 of the 221 recombinant inbred lines, and subsequent tests attributed the skew to failure of Y-bearing sperm to fertilize the eggs. Apparently these introgressed lines fail to suppress a normally silent meiotic drive system. Using molecular markers we mapped two regions of the Drosophila genome that appear to exhibit differences between D. simulans and D. sechellia in their regulation of sex chromosome segregation distortion. The data indicate that the sex ratio phenotype results from an epistatic interaction between at least two factors. We discuss whether this observation is relevant to the meiotic drive theory of hybrid male sterility.

Animals↗
PubMed1987

Segregation after mitotic crossing-over in isodicentric X chromosomes.

Segregation after mitotic crossing-over in an isodicentric (idic) X chromosome with one active and one inactive centromere has given rise to two new cell lines, one in which the idic(Xpter) chromosome has two active centromeres (most of these chromosomes also have an inversion) and another in which neither centromere is active. The two X chromosomes are attached at the telomeres of their short arms. Similar segregation has given rise to two other cell lines with idic(Xq-) chromosomes. Other observations on segregation after mitotic crossing-over are reviewed. Unequal crossing-over has apparently played a major role in the evolution of various genes and heterochromatin. Retinoblastoma and Wilms tumor are in some cases associated with homozygosity of a chromosome segment resulting from mitotic crossing-over. Similarly, the high incidence of cancer in Bloom syndrome may be caused by mitotic crossing-over leading to homozygosity or amplification of oncogenes.

Amenorrhea↗