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PubMedDate not supplied

[Peripheral material, or matrix, of mitotic chromosomes: structure and properties].

Peripheral chromosomal material carries a lot of protein components, enzymes, and factors into new nuclei and enables recommencement of both synthesis and assembly of ribosomes and synthesis of messenger RNA. A mitotic chromosome transfers to a new nuclei not only genetic information as chromatin DNA but also essential components of the synthetic apparatus ready for activation of transcription in a new cell cycle. The chromosome during cell division omnis mea meum porto.

Animals↗
PubMed1978

The 75 S RNA transcription unit in Balbiani ring 2 and its relation to chromosome structure.

A defined transcription unit in the Balbiani ring 2 (BR 2) region of chromosome IV in the salivary glands of Chironomus tentans has been characterized on the basis of analysis of the corresponding primary transcript, 75S RNA, and its functional significance. The available information on the transcription unit and its relations to chromosome structure can be summarized in the following way: 1. The size of the 75S RNA transcription unit in BR 2 is on the order of 30 000 base pairs. 2. The unit is likely to contain a long coding segment (at least 6000 base pairs), probably corresponding to information for salivary polypeptides. 3. The sequences are distributed in more than one chromomere (probably in 3--5 chromomeres). Further studies are needed before it can be stated whether or not there is a simple one-to-one relation between chromomeres and transcription units in the BR 2 region.

Animals↗
PubMed1977

Fluorescent probes of chromosome structure and replication.

Procedures employing fluorescent dyes or Giemsa stain have been utilized to differentiate methaphase chromosomes into longitudinal segments termed bands. In spite of the immense practical utility of chromosome banding, the chemical basis of banding patterns remains incompletely understood. Physical chemical studies have elucidated the modes and specificities of the interaction of fluorescent dyes such as quinacrine, 33258 Hoechst, daunomycin, chromomycin A3 and 7-aminoactinomycin D with DNA and chromatin. However, it is not clear that all aspects of chromosome staining are explainable in terms of the optical properties of soluble dye-DNA complexes. BrdU-dye techniques in which chromosome staining depends on the schedule of BrdU incorporation by cells, have been used for cytological studies of chromosome structure and replication. These procedures have revealed a close association between quinacrine or Giemsa bands and late replicating chromosomal regions. Biochemical studies on chromatin differentially labelled according to replication timing may thus prove useful for investigating the molecular basis of chromosome banding.

Animals↗
PubMed1994

Track structure, chromosome geometry and chromosome aberrations.

The joint role of radiation track structure and chromosome geometry in determining yields of chromosome aberrations is discussed. Ideally, the geometric models of chromosomes used for analyzing aberration yields should have the same degree of realism as track structure models. However, observed chromosome aberrations are produced by processes on comparatively large scales, e.g., misrepair involving two DSB located on different chromosomes or two DSB separated by millions of base pairs on one chromosome, and quantitative models for chromatin on such large scales have to date almost never been attempted. We survey some recent data on large-scale chromosome geometry, mainly results obtained with fluorescence in situ hybridization ("chromosome painting") techniques. Using two chromosome models suggested by the data, we interpret the relative yields, at low and high LET, of inter-chromosomal aberrations compared to intra-chromosomal, inter-arm aberrations. The models consider each chromosome confined within its own "chromosome localization sphere," either as a random cloud of points in one model or as a confined Gaussian polymer in the other. In agreement with other approaches, our results indicate that at any given time during the G0/G1 part of the cell cycle a chromosome is largely confined to a sub-volume comprising less than 10% of the volume of the cell nucleus. The possible significance of the ratio of inter-chromosomal aberrations to intra-chromosomal, inter-arm aberrations as an indicator of previous exposure to high LET radiation is outlined.

Cell Cycle↗
PubMed1980

Bleomycin-induced structural chromosomal aberrations in spermatogonia and bone-marrow cells of mice.

The induction of structural chromosomal aberrations by bleomycin (BLM) was studied in bone-marrow cells and spermatogonia of the mouse at doses of 10, 20, 40 and 80 mg/kg. BLM induced genetically important reciprocal translocations in stem-cell spermatogonia as measured with the spermatocyte test, and the response of bone-marrow cells to BLM was not markedly different from that of spermatogonia.

Animals↗
PubMed2005

Non-random structural chromosomal changes in ovarian cancer: i(5p) a novel recurrent abnormality.

Ovarian cancer represents the leading cause of death among patients with gynecological cancer. The genetic changes underlying the initiation and progression of ovarian cancer have not been well defined. However, non-random structural chromosomal changes have been identified with common chromosomal breakpoints. We have studied cytogenetically 15 cases of ovarian adenocarcinomas by a direct culture of cancer cells and a G-banding technique investigating the presence of recurrent structural aberrations with common chromosomal breakpoints. Among very complex structural rearrangements found, we could recognize recurrent structural aberrations involving according to frequency chromosomal regions 3p13-14, 11p15, 19q13, 3q21, 11q23, 11q10, 1p13, 1p36, and 17q24-25. Isochromosomes i(5p), i(17q), i(8q) and i(11q) were also observed. Isochromosome i(5p), rarely reported in ovarian cancer was found in seven cases suggesting that it may be a novel recurrent abnormality. Translocations t(1;11), t(3;19), t(3;17), t(7;11) and t(11;17) were also identified. Conventional cytogenetics continues to be valuable detecting the presence of non-random chromosomal breakpoints and facilitating the identification of genes implicated in tumorigenesis.

Adenocarcinoma↗
PubMed1990

Parental origin and mechanism of formation of X chromosome structural abnormalities: four cases determined with RFLPs.

Parental origin and mechanism of formation of X chromosome structural abnormalities were studied in one each case of dup(X)(pter----p11.4::p22.1----qter), del(X)(qter----p11:), i(X)(qter----cen----qter), and inv dup(X) (pter----q22::q22----pter) using various X-linked RFLPs as genetic markers. Segregation and densitometric analyses on polymorphic DNAs revealed that the dup(Xp) and the del(Xp) are both of paternal origin and the i(Xq) and i dic(X) are of maternal origin. The dup(Xp) had arisen by an unequal sister chromatid exchange and the del(Xp) had occurred through an intrachromosomal breakage-reunion mechanism, both in the paternal X chromosome. The i(Xq) had arisen either through centromere fission of a maternal X chromosome, followed by duplication of its long-arm, or through a translocation between two maternal X chromosomes after meiotic crossing-over. The inv dup(X) arose through sister chromatid breakage and reunion in a maternal X chromosome. These results, together with those of previous studies, suggest that the de novo abnormalities due to events involving centromere disruption arise predominantly during oogenesis, while those due to simple breakage-reunion events occur preferentially during spermatogenesis.

Child, Preschool↗
PubMed1990

Significance of structural chromosome aberrations in human sperm: analysis of induced aberrations.

A significant increase in the incidence of structural chromosome anomalies has been observed in the sperm of patients treated with radio and/or chemotherapy for different types of cancer when analyzed by the interspecific fertilization of hamster eggs. The analysis of these aberrations shows that while in controls only 9.4% of structural abnormalities are of the stable type, in treated patients this figure increases to 39.3%, thus indicating that the anomalies have not been produced during the fertilization of the hamster egg. However, it is possible that part, or even most, of the breaks appear as a result of a reduced repair capacity of sperm chromosomes in the cytoplasm of the hamster egg.

Antineoplastic Agents↗
PubMed2001

The Drosophila Su(var)2-10 locus regulates chromosome structure and function and encodes a member of the PIAS protein family.

The conserved heterochromatic location of centromeres in higher eukaryotes suggests that intrinsic properties of heterochromatin are important for chromosome inheritance. Based on this hypothesis, mutations in Drosophila melanogaster that alter heterochromatin-induced gene silencing were tested for effects on chromosome inheritance. Here we describe the characterization of the Su(var)2-10 locus, initially identified as a Suppressor of Position-Effect Variegation. Su(var)2-10 is required for viability, and mutations cause both minichromosome and endogenous chromosome inheritance defects. Mitotic chromosomes are improperly condensed in mutants, and polytene chromosomes are structurally abnormal and disorganized in the nucleus. Su(var)2-10 encodes a member of the PIAS protein family, a group of highly conserved proteins that control diverse functions. SU(VAR)2-10 proteins colocalize with nuclear lamin in interphase, and little to no SU(VAR)2-10 is found on condensed mitotic chromosomes. SU(VAR)2-10 is present at some polytene chromosome telomeres, and FISH analyses in mutant polytene nuclei revealed defects in telomere clustering and telomere-nuclear-lamina associations. We propose that Su(var2-10 controls multiple aspects of chromosome structure and function by establishing/maintaining chromosome organization in interphase nuclei.

Animals↗
PubMed2001

The human gephyrin (GPHN) gene: structure, chromosome localization and expression in non-neuronal cells.

Gephyrin was first described as a peripheral membrane protein of 93 kDa anchoring the glycine receptor (GlyR) to subsynaptic microtubules and cytoskeleton. Analysis of knock-out mice demonstrated that gephyrin has additional functions in GABA(A) receptor localization at the synapse and in the biosynthetic pathway of the molybdenum cofactor (Moco). Here we describe a human non-neuronal gephyrin cDNA and the exon/intron organization of the human gephyrin gene. We found the coding region to consist of 27 exons and to span approximately 800 kb on the long arm of chromosome 14. This structure is almost identical to that of the mouse gephyrin gene except that sequences corresponding to three exons described in rat and mouse could not be identified in human. Mutations of the GlyR subunits and of gephyrin lead to severe neuromotor phenotypes in human and mouse. Hyperekplexia involves most frequently a mutation in the GlyR alpha1 subunit in humans. However, inactivation of the Moco biosynthesis pathway results in very similar symptomatology. The recent characterization of a deletion of two exons of the gephyrin gene in a patient with symptoms typical of Moco deficiency confirmed that the involvement of gephyrin in these pathologies cannot be excluded. The precise localization of the gephyrin gene allowed us to exclude it from being a candidate for the autosomal dominant spastic paraplegia, the locus of which maps to 14q between markers D14S259 and D14S1018. A description of its structure and exon boundaries should lay the groundwork for further analysis of its expression in humans.

Animals↗
PubMed1999

The pattern of replication at a human telomeric region (16p13.3): its relationship to chromosome structure and gene expression.

We have studied replication throughout 325 kb of the telomeric region of a human chromosome (16p13.3) and related the findings to various aspects of chromosome structure and function (DNA sequence organization, nuclease-hypersensitive sites, nuclear matrix attachment sites, patterns of methylation and gene expression). The GC-rich isochore lying adjacent to the telomere, which contains the alpha-globin locus and many widely expressed genes, replicates early in the cell cycle regardless of the pattern of gene expression. In subtelomeric DNA, replication occurs later in the cell cycle and the most telomeric region (20 kb) is late replicating. Juxtaposition of early replicating DNA next to the telomere causes it to replicate later in S-phase. Analysis of the timing of replication in chromosomes with deletions, or in transgenes containing various segments of this telomeric region, suggests that there are no critical origins or zones that initiate replication, rather the pattern of replication appears to be related to the underlying chromatin structure which may restrict or facilitate access to multiple, redundant origins. These results contrast with the pattern of replication at the human beta-globin locus and this may similarly reflect the different chromosomal environments containing these gene clusters.

Animals↗
PubMed2003

[Alteration of chromosome structure in ovarian nurse cells of Drosophila melanogaster by hybrid dysgenesis].

The impact of hybrid dysgenesis on the chromosome structure of Drosophila melanogaster ovarian nurse cells was studied. In the examined lines and interlinear hybrids (including those yielded by dysgenic crosses in the P-M and I-R systems of hybrid dysgenesis), disturbed chromosome synapsis was revealed. The disturbance was somewhat similar to that observed in interspecific hybrids. Quantitative analysis showed that the mean frequency of nuclei with defective chromosome pairing ranged from 60.4 to 76%. FISH analysis of ovarian nurse chromosomes of Canton S x Berlin hybrids showed differences in the label localization in asynaptic homologs of arm 2L, which probably results in disrupted homolog pairing and reveal interlinear differences in localization of mobile genetic elements. Our results conform to Sved's model stating that hybrid dysgenesis is based on disorganization of the germline nuclear space.

Animals↗
PubMed2003

Cell-cycle-regulated expression and subcellular localization of the Caulobacter crescentus SMC chromosome structural protein.

Structural maintenance of chromosomes proteins (SMCs) bind to DNA and function to ensure proper chromosome organization in both eukaryotes and bacteria. Caulobacter crescentus possesses a single SMC homolog that plays a role in organizing and segregating daughter chromosomes. Approximately 1,500 to 2,000 SMC molecules are present per cell during active growth, corresponding to one SMC complex per 6,000 to 8,000 bp of chromosomal DNA. Although transcription from the smc promoter is induced during early S phase, a cell cycle transcription pattern previously observed with multiple DNA replication and repair genes, the SMC protein is present throughout the entire cell cycle. Examination of the intracellular location of SMC showed that in swarmer cells, which do not replicate DNA, the protein forms two or three foci. Stalked cells, which are actively engaged in DNA replication, have three or four SMC foci per cell. The SMC foci appear randomly distributed in the cell. Many predivisional cells have bright polar SMC foci, which are lost upon cell division. Thus, chromosome compaction likely involves dynamic aggregates of SMC bound to DNA. The aggregation pattern changes as a function of the cell cycle both during and upon completion of chromosome replication.

Bacterial Proteins↗