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PubMed1988

Chromosomal aberration and sister-chromatid exchange frequencies in peripheral blood lymphocytes of a large human population sample.

In order to assess the potential of cytogenetic determinations on peripheral blood lymphocytes as a means of monitoring human populations subject to low level occupational and environmental exposures to chemical mutagens and carcinogens, accurate baseline data are required. Accordingly, we have determined mean frequencies of chromosomal aberrations and of sister-chromatid exchanges, their variances, and the sources of this variance in a cohort of 353 healthy employees of the Brookhaven National Laboratory. A detailed protocol was adopted for blood sampling, lymphocyte culture, cytogenetic preparation and scoring in order to minimize variation from these potential sources. Scoring was divided between the Oak Ridge and the Brookhaven groups with duplicate scoring sufficient to evaluate and minimize the effect of any differences between laboratories or between individual scorers. In all, the data include 71,950 cells scored for chromosomal aberrations and 16,898 cells scored for sister-chromatid exchanges. The mean unadjusted frequency of sister-chromatid exchanges was 8.29 +/- 0.08/cell. As reported in other studies, cigarette smoking very significantly influenced sister-chromatid exchange frequencies; in our study the mean for smokers was 9.0 +/- 0.2, while that for non-smokers was 8.1 +/- 0.1/cell. The mean frequency was statistically higher in females than in males, regardless of smoking status. On the other hand, age of the subject did not significantly influence sister-chromatid exchange frequencies. Curiously, the subject's total white cell count did influence sister-chromatid exchange frequency. No other source of variation was found. The frequencies of chromosomal aberrations of all types were determined. The frequency of the most common unequivocal chromatid type, the chromatid deletion, was 0.81 +/- 0.05%, that of the most common unequivocal chromosome type, the dicentric, was 0.16 +/- 0.02%. No statistically significant influence was found of age or sex, nor of any other parameter tested, on the frequency of any chromosomal aberration type, with the single exception of long acentric fragments, often "supernumerary", believed to represent X chromosomes precociously separated at the centromere. Such fragments were significantly more frequent in samples from females than those from males, and showed a significant positive regression on age.

Aneuploidy↗
PubMed1991

The spindle is required for the process of sister chromatid separation in Drosophila neuroblasts.

We have studied two aspects of the process of sister chromatid separation in the Drosophila melanogaster neuroblasts. First, we analyzed the requirement of a functional spindle for sister chromatid separation to take place using microtubule depolymerizing drugs such as colchicine or a reversible analogue (MTC). Incubation of this tissue in colchicine causes the cells to block irreversibly at metaphase and no significant levels of sister chromatid separation were observed even after long periods of incubation. Exposure of neuroblasts to MTC also causes cells to block at metaphase, but after reversion most of the cells enter anaphase and are thus able to complete sister chromatid separation. These results imply that a functional spindle is required for sister chromatid separation. Second, we studied the role of heterochromatin during chromatid pairing and subsequent separation in chromosomes which carry either one or two extra pieces of heterochromatin. The results indicate that sister chromatids establish strong pairing along the translocated heterochromatin. During the early stages of anaphase, these chromosomes separate first the centromeric region and later the regions bearing extra heterochromatin. These results indicate that constitutive heterochromatin plays an important role for sister chromatid pairing and might be involved in the process of separation.

Animals↗
PubMed1975

The induction of chromatid deletions in accord with the breakage-and-reunion hypothesis.

In the present experiments it has been possible to study large numbers of X-ray induced chromatid deletions, or breads, in Chinese hamster chromosomes and to discern whether or not a sister chromatid exchange also occurs at the point of breadage. Chromatid deletions are only infrequently associated with a sister chromatid exchange. This is contrary to the expectations derived from the exchange hypothesis of Revell. Pn the basis of this hypothesis, in which chromatid deletions are considered to be incomplete exchanges that occur in the necks of little loops in the chromosomes, 40% of the chromatid breaks are expected to be associated with sister chromatid exchanges. The present data are in accord with the conclusions drawn from the earlier autoradiographic experiments of HEDDLE AND BODYCOTE, and show that chromatide breaks can be accounted for on the basis of the breakage-and reunion hypothesis, with the majority being simple breaks and some being incomplete exchanges between two such breaks.

Animals↗
PubMed1991

Abnormal sister-chromatid exchange induction by 3-aminobenzamide in an SV40-transformed Indian muntjac cell line: relationships with DNA maturation and DNA-strand breakage.

In SVM cells, an SV40-transformed line of Indian muntjac fibroblasts, levels of sister-chromatid exchanges are known to be abnormally high after UV-irradiation or alkylation. The SVM line is also known to have a defect in the processing of DNA-strand breaks. Sister-chromatid exchange in other cells is known to be stimulated by the poly(ADP-ribose) transferase inhibitor, 3-aminobenzamide, which also retards DNA-break sealing. Sister-chromatid exchanges in SVM cells are found to be hypersensitive to 3-aminobenzamide, or to nicotinamide deprivation which similarly inhibits poly(ADP-ribosyl)ation; DNA-strand breaks are likewise induced by 3-aminobenzamide. Bromodeoxyuridine, needed to detect sister-chromatid exchanges, is more toxic to SVM cells and itself induces sister-chromatid exchanges to a greater extent than it does in normal muntjac cells. However, in contrast to the situation reported for other cell types prone to sister-chromatid exchange (the Chinese hamster ovary mutant EM9 and human Bloom's Syndrome cells), SVM cells do not show an abnormal delay in DNA maturation when, under the influence of bromodeoxyuridine and 3-aminobenzamide, they show a high level of sister-chromatid exchange. The mechanism by which BrdU exerts its effects can largely be explained in terms of familiar effects on deoxyribonucleotide pools and DNA integrity. 3-Aminobenzamide, however, induces sister-chromatid exchanges in SVM cells by another mechanism.

Animals↗
PubMed1996

GFP tagging of budding yeast chromosomes reveals that protein-protein interactions can mediate sister chromatid cohesion.

BACKGROUND: Precise control of sister chromatid separation is essential for the accurate transmission of genetic information. Sister chromatids must remain linked to each other from the time of DNA replication until the onset of chromosome segregation, when the linkage must be promptly dissolved. Recent studies suggest that the machinery that is responsible for the destruction of mitotic cyclins also degrades proteins that play a role in maintaining sister chromatid linkage, and that this machinery is regulated by the spindle-assembly checkpoint. Studies on these problems in budding yeast are hampered by the inability to resolve its chromosomes by light or electron microscopy. RESULTS: We have developed a novel method for visualizing specific DNA sequences in fixed and living budding yeast cells. A tandem array of 256 copies of the Lac operator is integrated at the desired site in the genome and detected by the binding of a green fluorescent protein (GFP)-Lac repressor fusion expressed from the HIS3 promoter. Using this method, we show that sister chromatid segregation precedes the destruction of cyclin B. In mad or bub cells, which lack the spindle-assembly checkpoint, sister chromatid separation can occur in the absence of microtubules. The expression of a tetramerizing form of the GFP-Lac repressor, which can bind Lac operators on two different DNA molecules, can hold sister chromatids together under conditions in which they would normally separate. CONCLUSIONS: We conclude that sister chromatid separation in budding yeast can occur in the absence of microtubule-dependent forces, and that protein complexes that can bind two different DNA molecules are capable of holding sister chromatids together.

Bacterial Proteins↗
PubMed1989

Fine-structural aspects of bromodeoxyuridine incorporation in sister chromatid differentiation and replication banding.

The structure of harlequin-stained chromosomes following substitution with low levels of 5-bromodeoxyuridine (BrdUrd) over two cell cycles and high levels over the last part of one cycle (replication banding) was studied in Chinese hamster ovary (CHO) cells. By using correlative light (LM) and scanning electron microscopy (SEM), it was shown that the effects of both the ultraviolet light (u.v.) and hot SSC treatment steps of the harlequin staining procedure were necessary to obtain sister-chromatid differentiation (SCD) or replication banding. u.v. treatment alone resulted in dark Giemsa staining of both chromatids with SEM morphology of short compact protuberances and an overall flattened smooth appearance in both the unsubstituted and BrdUrd-substituted chromatids, a morphology essentially similar to that of untreated chromosomes. SSC alone on the other hand resulted in dark-staining chromatids with an SEM morphology of raised, loosely packed loops of fibres in both types of chromatids. u.v. and SSC treatment together resulted in differentiation, with dark-staining unifilarly (TB) chromatids in the LM corresponding to raised loosely packed loops in the SEM and pale bifilarly (BB) chromatids corresponding to the smooth compact flattened SEM appearance. Where the BrdUrd-substituted strand became the template (BT), or when the nascent strand TB contained high levels of BrdUrd substitution in replication banding, the chromatid stained pale and showed the compact smooth appearance in the SEM. The Giemsa staining ability and ultrastructural morphology of harlequin staining is discussed with respect to putative DNA loss and also in terms of preferential protein-protein, protein-DNA cross-linkage in BrdUrd-containing DNA. These changes are also compared with the ultrastructural morphology observed after other banding methods, where deterioration of protein and DNA-protein interaction resulting in aggregation of chromatin fibres appears to be the major mechanism.

Animals↗
PubMed1979

Sister chromatid exchange induction resulting from systemic, topical, and systemic-topical presentations of carcinogens.

Chinese hamster cheek pouch mucosal cells were examined for in vivo sister chromatid exchange formation resulting from the exposure of animals to carcinogens presented in three manners: systemic, topical, and systemic-topical combination. The systemic presentation of cyclophosphamide (5 or 10 mg/kg) through i.p. injection resulted in an increase in sister chromatid exchanges from 4.8 to 9.9 per cell. Topical application of 7,12-dimethylbenz(a)anthracene (0.5% in mineral oil, 0.1 ml) resulted in an increase in the sister chromatid exchange frequency to 11.5/cell, as compared with a value of 5.0/cell in animals treated only with mineral oil. Systemic administration of 8-methoxypsoralen (0.5, 1, 2.5, or 5 mg/kg) through i.p. injection, followed by activation with topical near-ultraviolet light (3.75 x 10(4) ergs/sq mm at 365 nm) resulted in an increase in sister chromatid exchange, reaching 15.4/cell at 5 mg 8-methoxypsoralen per kg. Exposure of animals to 8-methoxypsoralen or near-ultraviolet light alone, but not in combination, did not produce an increase in sister chromatid exchange. Sister chromatid exchange frequencies in cheek pouch cells were also compared with sister chromatid exchange frequencies in marrow cells of identically treated animals to assess the importance of exposure mode and tissue specificity in sister chromatid exchange formation.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1986

Chromatid behavior in late mitosis: a scanning electron microscopy analysis of mammalian cell lines with various chromosome numbers.

Chromatid activity during the process of nuclear reformation following metaphase is a period of mitosis where little precise information is available. Nuclear reformation requires that chromosomes, at metaphase and chromatids during anaphase and telophase align, position and associate in a clearly defined sequence to insure the specific design of each nucleus. Four cell lines with chromosome numbers ranging from seven to almost seventy were chosen to determine whether the process of nuclear assembly is the same throughout. Chromosomal alignment at metaphase is found to be radial in all four cell lines. Chromosome positioning is essentially the same in all four, where the smaller chromosomes are located centrally and longer ones are positioned peripherally in a radial alignment. Chromosomal association is directly related to chromosome number. The more chromosomes in a one dimensional plane occupying a given area, the closer the association. In comparing the HeLaS3 and muntjac chromatids, the former has the closer association at metaphase. Since association is the most important aspect of chromatid behavior in nuclear reformation, chromatid positioning becomes a vital process during anaphase movement. Chromatid positions established during anaphase determines later positioning in the interphase nucleus because of the subsequent interconnection of adjacent chromatids by the formation of a fibrous meshwork. This fibrous meshwork, formed in anaphase and early telophase, functions to stabilize chromatids following their positioning and it also serves as a substrate or matrix for the assembly of nuclear envelope.

Anaphase↗
PubMed1980

Susceptibility to fluorescent light-induced chromatid breaks associated with DNA repair deficiency and malignant transformation in culture.

The increased susceptibility of mouse cells to fluorescent light-induced chromatid damage following their spontaneous malignant transformation in culture could result from loss or inactivation of catalase that decomposes the photoproduct H2O2 or from impaired capacities to repair DNA damage. No consistent change in catalase activity with respect to neoplastic state could be established. To interpret the cytogenetic damage in terms of DNA strand breaks, we determined the incidence of chromatid breaks induced by light exposure during the G1 and late S-G2 phases of the cell cycle in normal and malignant derivatives of a C3H mouse cell line. Chromatid breaks at metaphase following light exposure during G1 would result from DNA strand breaks, cross-links, or base damage, whereas breaks following exposure during late S-G2 would result from single-or double-strand breaks. Both G1 and late S-G2 were susceptible in malignant cells but only G1 in normal. Since caffeine inhibits DNA repair, we compared its effects on light-induced chromatid damage in the normal and malignant cells to assess their DNA repair capacities. Treatment of normal cells with caffeine (50 microgram/ml) directly following five hr of light exposure in G1 increased the chromatid damage to that in malignant cells exposed with or without caffeine. Similarly, treatment of normal cells with caffeine during late S-G2 exposure increased chromatid damage to a level not significantly different from that in malignant cells exposed without caffeine. Caffeine had little influence on chromatid damage in malignant cells. The increased susceptibility of malignant mouse cells to fluorescent light-induced chromatid breaks thus appears to result from impaired capacities to repair DNA damage.

Animals↗
PubMed2003

Condensin-dependent localisation of topoisomerase II to an axial chromosomal structure is required for sister chromatid resolution during mitosis.

Assembly of compact mitotic chromosomes and resolution of sister chromatids are two essential processes for the correct segregation of the genome during mitosis. Condensin, a five-subunit protein complex, is thought to be required for chromosome condensation. However, recent genetic analysis suggests that condensin is only essential to resolve sister chromatids. To study further the function of condensin we have depleted DmSMC4, a subunit of the complex, from Drosophila S2 cells by dsRNA-mediated interference. Cells lacking DmSMC4 assemble short mitotic chromosomes with unresolved sister chromatids where Barren, a non-SMC subunit of the complex is unable to localise. Topoisomerase II, however, binds mitotic chromatin after depletion of DmSMC4 but it is no longer confined to a central axial structure and becomes diffusely distributed all over the chromatin. Furthermore, cell extracts from DmSMC4 dsRNA-treated cells show significantly reduced topoisomerase II-dependent DNA decatenation activity in vitro. Nevertheless, DmSMC4-depleted chromosomes have centromeres and kinetochores that are able to segregate, although sister chromatid arms form extensive chromatin bridges during anaphase. These chromatin bridges do not result from inappropriate maintenance of sister chromatid cohesion by DRAD21, a subunit of the cohesin complex. Moreover, depletion of DmSMC4 prevents premature sister chromatid separation, caused by removal of DRAD21, allowing cells to exit mitosis with chromatin bridges. Our results suggest that condensin is required so that an axial chromatid structure can be organised where topoisomerase II can effectively promote sister chromatid resolution.

Adenosine Triphosphatases↗
PubMed1982

Extracentromeric connections between sister chromatids demonstrated in human chromosomes induced to condense asymmetrically.

Extracentromeric chromatin fibers were proposed to hold sister chromatids together in mitotic chromosomes examined by electron microscopy, but their existence in living cells has not been demonstrated yet. We have performed an in vitro BrdU-H33258 treatment which induced a differential rate of condensation to each sister chromatid, thus producing asymmetrically condensing chromosomes. The fast condensing chromatid pulled the slower sister one, both bending in parallel. Bent chromatids appeared reciprocally connected by loops of chromatin fibers, suggesting they were the links which permitted the physical interplay between the differently condensing chromatids. When sister chromatid exchanges (SCE) intercalated a fast-condensing fragment in the slow-condensing chromatid or vice versa, the chromosome inverted its curvature at the SCE-point.

Chromatids↗
PubMed1998

The signal model: a possible explanation for the conversion of DNA double-strand breaks into chromatid breaks.

PURPOSE: To present and evaluate the 'signal' model for the formation of radiation-induced chromatid breaks. CONCLUSIONS: Chromatid breaks in human cells represent the apparent interstitial loss of up to about 40 Mbp of DNA, difficult to account for as single lesions under the classical 'breakage-and-reunion' hypothesis. If breakage-first resulted from two interacting DNA double-strand breaks (dsb) with the loss or displacement of the intervening fragment, a dose-squared relationship would be predicted for chromatid breaks. However, the relationship between chromatid break frequency and dose for human cells is linear. The alternative 'exchange' model of Revell is based on the principle of the interaction of two initiating lesions, thus also predicting a dose-squared relationship for chromatid 'breaks'. The signal model explains the conversion of dsb into chromatid breaks on the assumption that a single dsb generates a signal which triggers the cell to initiate a recombinational exchange involving a large loop of chromatin. Incomplete exchanges would be observed as chromatid breaks. Possible candidates for the signalling molecule(s) are DNA protein kinase (DNA PK) and the ATM protein.

Animals↗
PubMed1994

Sister chromatid separation and the metaphase-anaphase transition in mouse oocytes.

The paper reports on the effect of experimentally inhibiting chromatid separation on meiotic progression and maturation-promoting factor (MPF) activity in both metaphase I (Experiment 1) and metaphase II mouse oocytes (Experiment 2) subjected to combinations of inhibitors of (a) protein synthesis, (b) topoisomerase II, and (c) cytokinesis-cytoskeleton integrity. The results from Experiment 1 showed that the inhibition of protein synthesis invariably results in the extrusion of the first polar body and the formation of an interphase nucleus. Furthermore, this inhibition induces a rapid decline in MPF activity. Similarly, in Experiment 2 the exposure of metaphase II oocytes to cycloheximide initiated a rapid fall in MPF activity, progression to anaphase, the extrusion of the second polar body, and the formation of a pronucleus. While the inhibition of protein synthesis hastened progression through the meiotic cycle, the opposite effect was observed when chromatid separation was prevented by etoposide or colcemid treatment. The results in Experiment 1 demonstrated that the inhibition of chromatid separation totally blocked meiotic progression by preventing the metaphase I to anaphase I transition. These oocytes were characterized by the persistence of high MPF activity for extended periods of time (> 20 hr). This activity declined slowly in oocytes exposed both to inhibitors of chromatin separation and protein synthesis. In Experiment 2 the results showed that the prevention of chromatin separation induced changes which paralleled those observed with MI oocytes. The prevention of chromatid separation with either etoposide or colcemid converted the oocytes from being sensitive to activation stimuli to being entirely resistant to standard activation. In addition, MPF activity remained persistently elevated and declined only when protein synthesis was inhibited. The decline in intracellular MPF activity reached basal levels 6 to 10 hr after the addition of cycloheximide and was accompanied by the slow and gradual decondensation of chromatin. Our results are in accord with those from recent experiments in yeast, insects, and amphibia which suggest that chromatid separation provides an essential signal for cell cycle progression beyond M-phase. We postulate first that exist from both metaphase I and metaphase II, and the characteristic reduction in MPF activity at anaphase in mouse oocytes, are initiated by chromosome (chromatid) separation. Second, we suggest that chemically induced chromosome (chromatid) separation block prevents the anaphase to telophase transition by inhibiting MPF degradation. Third, we postulate that the slow escape from metaphase arrest in oocytes treated with both etoposide and cycloheximide reflects a gradual decrease of MPF activity due to normal protein turnover without new synthesis.

Anaphase↗
PubMed1985

Nuclear reformation following metaphase in HeLa S3 cells: three-dimensional visualization of chromatid rearrangements.

Nuclear reformation from chromatids following metaphase was visualized three-dimensionally for the first time in mammalian cells (HeLa S3) by scanning electron microscopy (SEM). Anaphase and telophase configurations free of mitotic apparatus, cytoskeletal elements and nuclear envelope were prepared using a slightly modified standard cytological procedure which permitted visualization of chromatid position and orientation. Mid-anaphase alignments were observed to be more complex than previously revealed by light and transmission electron microscopy (TEM). One pole consisted of chromatids joined along their lateral length, the other pole consisted of telomeres, apparently of the longest chromatids, aligned in a double concentric layer. As anaphase progressed, re-association of these chromatids appeared to occur progressively along their lateral length toward their telomeres. Morphological evidence is presented suggesting that this lateral re-association may involve interchromatid fibers. After complete joining, structures resembling a hollow half sphere had formed. Based on different preparative procedures for SEM and published TEM analysis, it is this shell-like configuration upon which the nuclear envelope is reestablished in early telophase. As telophase progressed there was loss in depth of the internal chamber resulting in a disc configuration. Following loss of chromatid outline from the surface of this structure, interphase nuclear shape was assumed. Morphometric determinations revealed relative dimensions of chromatid configurations and supported the conclusion that nuclear reformations proceeded by discrete steps. The complexity of such a process, as revealed by SEM analysis, is discussed.

Cell Cycle↗
PubMed1996

The diplochromosome of endoreduplicated cells: a new approach to highlight the mechanism of sister chromatid exchange.

Chinese hamster lung embryonic cells (CL1) were treated with colchicine in order to induce endoreduplication and subsequently with mitomycin-C (MMC) to induce exchanges within the diplochromosome. The use of chromosomal differential staining through incorporation of 5-bromodeoxyuridine, resulting in only one stained chromatid, has allowed the analysis of all classes of exchanges among the four chromatids of the diplochromosome. Three classes of exchanges may occur: intradiplochromatid exchanges (ICEs) between the two inner chromatids, cousin chromatid exchanges (CCEs) between one inner and one outer chromatid, and sister chromatid exchanges (SCEs) between the two sister chromatids of the diplochromosome. The results show that MMC treatment, in the last cell cycle of endoreduplication, as expected, significantly increases only the frequency of SCEs, whereas the frequency of ICEs and CCEs remains unchanged. This result supports replication models of formation of SCEs. Furthermore the fact that the number of ICEs does not increase means that the molecular mechanism of somatic crossing over is not related to that of SCE formation, or very rarely. The results also indicate a statistically significant lower induction of SCEs in endoreduplicated metaphases as compared with diploid ones both in control and MMC-treated cells. Such a result may be due to structural restrictions within the diplochromosome.

Animals↗
PubMed1991

Sister chromatid exchange frequency in directly prepared cytotrophoblasts: demonstration of in vivo deoxyribonucleic acid damage in pregnant women who smoke cigarettes.

Assessing frequency of sister chromatid exchange is a sensitive method of monitoring exposure to clastogens, mutagens, and other substances that induce deoxyribonucleic acid damage. Aware that cigarette smoke is associated with increased sister chromatid exchange in many cell types, we sought to determine whether an in vivo effect of cigarette smoke could be demonstrated by study of sister chromatid exchange in chorionic villus cells. Directly prepared cytotrophoblasts and cultured mesenchymal core cells were analyzed. Mean sister chromatid exchange frequency in cytotrophoblasts from smoking subjects (8.87 sister chromatid exchanges per cell) was significantly greater than in nonsmoking subjects (5.81 sister chromatid exchanges per cell; p less than 0.001); however, no significant difference in cultured mesenchymal core cells was found. Our results demonstrate that maternal exposure to cigarette smoke results in direct placental deoxyribonucleic damage, which in turn could explain deleterious effects of smoking on pregnancy. Increased sister chromatid exchange frequency was observed only in directly prepared cytotrophoblasts, showing the necessity of using this cell type to evaluate the effects of clastogens on placentas.

Chorionic Villi↗
PubMed1985

Chromatid damage induced by fluorescent light during G2 phase in normal and Gardner syndrome fibroblasts. Interpretation in terms of deficient DNA repair.

Skin fibroblasts from Gardner syndrome (GS) compared with those from normal donors showed a significantly higher incidence of chromatid gaps and breaks following exposure to low-intensity, cool-white fluorescent light during G2 phase of the cell cycle. Considerable evidence supports the concept that chromatid gaps and breaks seen directly after exposure to DNA-damaging agents represent unrepaired DNA single- and double-strand breaks respectively. The changes in incidence of chromatid aberrations with time after light exposure are consistent with the sequence of events known to follow DNA damage and repair. Initially, the incidence of light-induced chromatid gaps was equivalent in GS and normal fibroblasts. In the normal cells, the chromatid gaps disappeared by 1 h post-exposure, presumably as a result of efficient repair of DNA single-strand breaks. In contrast, the incidence of gaps increased in GS cells by 0.5 h followed by a decrease at 1 h and concomitant increase in chromatid breaks. It appears from these findings that the increased incidence of chromatid damage in GS fibroblasts results from deficient repair of DNA single-strand breaks which arise from incomplete nucleotide excision of DNA damage during G2 phase.

Cells, Cultured↗
PubMed1999

Competence for assembly of sister chromatid cores is progressively acquired during S phase in mammalian cells.

Condensed sister chromatids possess a protein scaffold or axial core to which loops of chromatin are attached. The sister cores are believed to be dynamic frameworks that function in the organization and condensation of chromatids. Chromosome structural proteins are implicated in the establishment of sister chromatid cohesion and in the maintenance of epigenetic phenomena. Both processes of templating are tightly linked to DNA replication itself. It is a question whether the structural basis of sister chromatid cores is templated during S phase. As cells proceed through the cell cycle, chromatid cores undergo changes in their protein composition. Cytologically, cores are first visualized at the start of prometaphase. Still, core assembly can be induced in G1 and G2 when interphase cells are fused with mitotic cells. In this study, we asked if chromatid cores are similarly able to assemble in S-phase cells. We find that the ability to assemble cores is transiently lost during local replication, then regained in chromosome regions shortly after they have been replicated. We propose that core templating occurs coincident with DNA replication and that the competence for the assembly of the sister chromatid cores is acquired shortly after passage of replication forks.

Animals↗