| 1. |
- Alfredsson-Timmins, Jenny, 1976-, et al.
(författare)
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Reorganization of chromatin is an early response to nitrogen starvation in Schizosaccharomyces pombe
- 2009
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Ingår i: Chromosoma. - : Springer Science and Business Media LLC. - 0009-5915 .- 1432-0886. ; 118:1, s. 99-112
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Tidskriftsartikel (refereegranskat)abstract
- There are several documented events of changes in subnuclear localization during gene activation. However, there are conflicting data on whether the nuclear periphery is a compartment for gene repression or activation, and whether genes are moved to the pores at the nuclear membrane (NM) or not during gene activation. Nitrogen starvation of fission yeast serves as a good model system for studying gene induction since it causes fast regulation of hundreds of genes. In this study the subnuclear localization of two gene clusters repressed by nitrogen was investigated. During normal growth conditions the gene clusters localized to the nuclear periphery at the opposite side of the nucleus as compared to the spindle pole body (SPB). This constrained localization was dependent on the histone deacetylase Clr3, known to transcriptionally repress genes in these clusters. Already 20 minutes after nitrogen depletion drastic changes in subnuclear localization of the two loci were observed, away from the NM towards the nuclear interior. At least for one of the clusters the movement was clearly transcription dependent. Data presented here illustrates how interconnected events of gene activation and nuclear reorganization are, as well as provides a suggestion of how nuclear organization might be maintained.
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| 2. |
- Block, K, et al.
(författare)
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Minichromosomes in Drosophila melanogaster derived from the transposing element TE1
- 1990
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Ingår i: Chromosoma. - : Springer. - 0009-5915 .- 1432-0886. ; 99:5, s. 336-343
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Tidskriftsartikel (refereegranskat)abstract
- A minichromosome has originated from the transposing element TE1. This autonomously replicating chromosome contains the structural genes white and roughest, from the Drosophila X chromosome. It arose within a stock carrying TE1 at 45F on chromosome 2. In addition to the w and rst genes, the minichromosome may carry section 45C-45F from chromosome 2. It is inherited by 33%-47% of the offspring. By this criterion it carries a centromere, although the origin of the centromere is unknown. From this minichromosome a still smaller one has originated, probably through the loss of all material from chromosome 2 together with some heterochromatin. At the same time a duplication of white and roughest could have taken place. This chromosome has a strange morphology and is more frequently lost in meiosis than the larger one, but is still transmitted to about 29%-37% of the progeny of one parent heterozygous for the minichromosome. In both cases the flies have variegated eyes, probably as a result of position-effect variegation. The variegation pattern is influenced by factors in the X chromosome. The size of the smaller minichromosome is little more than 1 Mb as determined by pulsed field gel electrophoresis.
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| 3. |
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| 4. |
- Ferretti, Ana B. S. M., et al.
(författare)
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How dynamic could be the 45S rDNA cistron? : An intriguing variability in a grasshopper species revealed by integration of chromosomal and genomic data
- 2019
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Ingår i: Chromosoma. - : SPRINGER. - 0009-5915 .- 1432-0886. ; 128:2, s. 165-175
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Tidskriftsartikel (refereegranskat)abstract
- To better understand the structure and variability of the 45S rDNA cistron and its evolutionary dynamics in grasshoppers, we performed a detailed analysis combining classical and molecular cytogenetic data with whole-genome sequencing in Abracris flavolienata, which shows extraordinary variability in the chromosomal distribution for this element. We found astonishing variability in the number and size of rDNA clusters at intra- and inter-population levels. Interestingly, FISH using distinct parts of 45S rDNA cistron (18S rDNA, 28S rDNA, and ITS1) as probes revealed a distinct number of clusters, suggesting independent mobility and amplification of the 45S rDNA components. This hypothesis is consistent with the higher genomic coverage of almost the entire cistron of 45S rDNA observed in A. flavolineata compared to other grasshoppers, besides coverage variability along the 45S rDNA cistron in the species. In addition, these differences in coverage for distinct components of the 45S rDNA cistron indicate emergence of pseudogenes evidenced by existence of truncated sequences, demonstrating the rDNA dynamics in the species. Although the chromosomal distribution of 18S rDNA was highly variable, the chromosomes 1, 3, 6, and 9 harbored rDNA clusters in all individuals with the occurrence of NOR activity in pair 9, suggesting ancestry or selective pressures to prevent pseudogenization of rDNA sequences in this chromosome pair. Additionally, small NORs and cryptic rDNA loci were observed. Finally, there was no evidence of enrichment and association of transposable elements, at least, inside or nearby rDNA cistron. These findings broaden our knowledge of rDNA dynamics, revealing an independent movement and amplification of segments of 45S rDNA cistron, which in A. flavolineata could be attributed to ectopic recombination.
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| 5. |
- Gisselsson Nord, David
(författare)
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Classification of chromosome segregation errors in cancer.
- 2008
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Ingår i: Chromosoma. - : Springer Science and Business Media LLC. - 0009-5915 .- 1432-0886. ; Jun 6, s. 511-519
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Tidskriftsartikel (refereegranskat)abstract
- Abnormal chromosome segregation at mitosis is one way by which neoplastic cells accumulate the many genetic abnormalities required for tumour development. In this paper, a straightforward morphology-based classification of chromosome segregation errors in cancer is suggested. This classification distinguishes between abnormalities in spindle symmetry (spindle multipolarity, size-asymmetry of ana-telophase poles) and abnormalities in sister chromatid segregation (chromosome bridges, chromatid bridges, chromosome lagging, acentric fragment lagging). Often, these categories of errors must be combined to accurately describe the events in a single abnormal mitotic cell. The suggested categories can to some extent be distinguished by standard chromatin staining. However, labelling of abnormal mitotic figures by fluorescence in situ hybridization and immunofluorescence enhances the accuracy of classification and also allows visualisation of the segregation of individual chromosomes, making it possible to detect non-disjunction also in the absence of gross alterations in mitotic morphology. Further characterisation of the molecular alterations leading to abnormal chromosome segregation together with the current developments in nano-level and real-time imaging will undoubtedly lead to an improved understanding of chromosome dynamics in cancer cells. Any morphology-based classification of chromosome segregation errors in cancer must therefore be taken as provisional, anticipating a satisfactory integration of morphology and molecular biology.
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| 6. |
- Gisselsson Nord, David, et al.
(författare)
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Interphase chromosomal abnormalities and mitotic missegregation of hypomethylated sequences in ICF syndrome cells
- 2005
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Ingår i: Chromosoma. - : Springer Science and Business Media LLC. - 0009-5915 .- 1432-0886. ; 114:2, s. 118-126
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Tidskriftsartikel (refereegranskat)abstract
- The immunodeficiency, centromeric region instability, facial anomalies (ICF) syndrome is a rare autosomal recessive disease. Usually, it is caused by mutations in the DNA methyltransferase 3B gene, which result in decreased methylation of satellite DNA in the juxtacentromeric heterochromatin at 1qh, 16qh, and 9qh. Satellite II-rich 1qh and 16qh display high frequencies of abnormalities in mitogen-stimulated ICF lymphocytes without these cells being prone to aneuploidy. Here we show that in lymphoblastoid cell lines from four ICF patients, there was increased colocalization of the hypomethylated 1qh and 16qh sequences in interphase, abnormal looping of pericentromeric DNA sequences at metaphase, formation of bridges at anaphase, chromosome 1 and 16 fragmentation at the telophase-interphase transition, and, in apoptotic cells, micronuclei with overrepresentation of chromosome 1 and 16 material. Another source of anaphase bridging in the ICF cells was random telomeric associations between chromosomes. Our results elucidate the mechanism of formation of ICF chromosome anomalies and suggest that 1qh-16qh associations in interphase can lead to disturbances of mitotic segregation, resulting in micronucleus formation and sometimes apoptosis. This can help explain why specific types of 1qh and 16qh rearrangements are not present at high frequencies in ICF lymphoid cells despite diverse 1qh and 16qh aberrations continuously being generated.
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| 7. |
- Gisselsson Nord, David, et al.
(författare)
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Variable stability of chromosomes containing amplified alpha-satellite sequences in human mesenchymal tumours
- 1999
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Ingår i: Chromosoma. - : Springer Science and Business Media LLC. - 0009-5915 .- 1432-0886. ; 108:5, s. 271-277
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Tidskriftsartikel (refereegranskat)abstract
- Alpha-satellite sequences are found in the centromeric region of all human chromosomes and have been implicated in centromeric function. We describe the structure and behaviour of chromosomes containing amplified human alphoid DNA from chromosome 12, in an osteosarcoma cell line (OSA) and an atypical lipomatous tumour (ALT). In OSA, the amplified material was detected in one large marker chromosome, whereas in ALT amplified sequences were observed in chromosomes of variable number and appearance. The marker in OSA was mitotically stable, but those in ALT exhibited a high degree of mitotic instability, forming bridges at anaphase and chromatin strings between interphase nuclei. The amplified alpha-satellite arrays reacted positively with human anti-centromeric antiserum and anti-centromere protein B antibodies in both tumours. Centromere protein C, previously shown to be present only in functional kinetochores, was invariably detected at the constriction of the marker in OSA, while one-fifth of markers in ALT appeared to exhibit additional centromere protein C-positive regions outside the primary constriction, indicating that the observed chromosomal instability in ALT might, at least in part, be a consequence of the occasional formation of more than one functional kinetochore. In OSA the alphoid DNA was coamplified with unique sequences from central 12q and the amplified material was C-band negative but in ALT amplified material from central 12q as well as sequences from proximal 12p were detected, resulting in C-band-positive areas. A propensity for additional kinetochore formation might thus be associated with the coamplification of alphoid DNA and pericentromeric sequences from chromosome 12.
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| 8. |
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| 9. |
- Kravchuk, Oksana, et al.
(författare)
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Transvection in Drosophila : trans-interaction between yellow enhancers and promoter is strongly suppressed by a cis-promoter only in certain genomic regions
- 2017
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Ingår i: Chromosoma. - : Springer Science and Business Media LLC. - 0009-5915 .- 1432-0886. ; 126:3, s. 431-441
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Tidskriftsartikel (refereegranskat)abstract
- Transvection is a phenomenon of interallelic communication whereby enhancers of one allele can activate a promoter located on the homologous chromosome. It has been shown for many independent genes that enhancers preferentially act on the cis-linked promoter, but deletion of this promoter allows the enhancers to act in trans. Here, we tested whether this cis-preference in the enhancer-promoter interaction could be reconstituted outside of the natural position of a gene. The yellow gene was chosen as a model system. Transgenic flies were generated that carried the yellow gene modified by the inclusion of the strategically placed recognition sites for the Cre and Flp recombinases. To facilitate transvection, an endogenous Su(Hw) insulator (1A2) or gypsy insulator was placed behind the yellow gene. Independent action of the recombinases produced a pair of derivative alleles, one containing the promoter-driven yellow gene, and the other, the enhancers and promoter that failed to produce a functional yellow protein. As a result, we observed strong transvection in many genomic regions, suggesting that a complete cis-preference of the enhancer-promoter interactions is mainly restricted to genes in their natural loci.
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| 10. |
- Kumar, Rajendra, et al.
(författare)
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Genomic 3D compartments emerge from unfolding mitotic chromosomes
- 2019
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Ingår i: Chromosoma. - : Springer. - 0009-5915 .- 1432-0886. ; 128:1, s. 15-20
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Tidskriftsartikel (refereegranskat)abstract
- The 3D organisation of the genome in interphase cells is not a randomly folded polymer. Rather, experiments show that chromosomes arrange into a network of 3D compartments that correlate with biological processes, such as transcription, chromatin modifications and protein binding. However, these compartments do not exist during cell division when the DNA is condensed, and it is unclear how and when they emerge. In this paper, we focus on the early stages after cell division as the chromosomes start to decondense. We use a simple polymer model to understand the types of 3D structures that emerge from local unfolding of a compact initial state. From simulations, we recover 3D compartments, such as TADs and A/B compartments that are consistently detected in chromosome capture experiments across cell types and organisms. This suggests that the large-scale 3D organisation is a result of an inflation process.
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