Condensin I and II behaviour in interphase nuclei and cells undergoing premature chromosome condensation

Zhang, Tao; Paulson, James R.; Bakhrebah, Muhammed; Kim, Ji Hun; Nowell, Cameron J.; Kalitsis, Paul; Hudson, Damien F.

doi:10.1007/s10577-016-9519-7

Cited by 31 publications

(28 citation statements)

References 80 publications

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“…CAP-H depleted cells have a much lower contact frequency between loci separated less than 6 Mb as compared to WT and CAP-H2 deleted cells. These observations suggest condensin I and II play distinct roles, and at different structural levels, in mitotic chromosome morphogenesis, providing a mechanistic explanation for earlier microscopic studies (57)(58)(59)(60).…”

Section: Condensin I and Ii Play Distinct Roles In Chromosome Morphogsupporting

confidence: 58%

Mitotic chromosomes fold by condensin-dependent helical winding of chromatin loop arrays

Samejima

Goloborodko

et al. 2017

Preprint

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During mitosis, chromosomes fold into compacted rod shaped structures. We combined imaging and Hi-C of synchronous DT40 cell cultures with polymer simulations to determine how interphase chromosomes are converted into compressed arrays of loops characteristic of mitotic chromosomes. We found that the interphase organization is disassembled within minutes of prophase entry and by late prophase chromosomes are already folded as arrays of consecutive loops. During prometaphase, this array reorganizes to form a helical arrangement of nested loops. Polymer simulations reveal that Hi-C data are inconsistent with solenoidal coiling of the entire chromatid, but instead suggest a centrally located helically twisted axis from which consecutive loops emanate as in a spiral staircase. Chromosomes subsequently shorten through progressive helical winding, with the numbers of loops per turn increasing so that the size of a helical turn grows from around 3 Mb (~40 loops) to ~12 Mb (~150 loops) in fully condensed metaphase chromosomes. Condensin is essential to disassemble the interphase chromatin conformation. Analysis of mutants revealed differing roles for condensin I and II during these processes. Either condensin can mediate formation of loop arrays. However, condensin II was required for helical winding during prometaphase, whereas condensin I modulated the size and arrangement of loops inside the helical turns. These observations identify a mitotic chromosome morphogenesis pathway in which folding of linear loop arrays produces long thin chromosomes during prophase that then shorten by progressive growth of loops and helical winding during prometaphase. One Sentence Summary:Mitotic chromosome morphogenesis occurs through condensin-mediated disassembly of the interphase conformation and formation of extended prophase loop arrays that then shorten by loop growth and condensin-dependent helical winding.

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Section: Condensin I and Ii Play Distinct Roles In Chromosome Morphogsupporting

confidence: 58%

Mitotic chromosomes fold by condensin-dependent helical winding of chromatin loop arrays

Samejima

Goloborodko

et al. 2017

Preprint

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“…During interphase, in vertebrates the most commonly described localization of condensin I is exclusively in the cytoplasm (Hirota et al, 2004;Ono et al, 2004;Gerlich et al, 2006;Hirano, 2012a). However, some reports regarding Drosophila, chicken and human cell cultures described the localization of condensin I additionally within the nucleus (Schmiesing et al, 2000;Savvidou et al, 2005;Zhang et al, 2016). In A. thaliana protoplasts and N. benthamiana epidermal leaves, we observed CAP-D2, CAP-G and CAP-H EYFP-fusion proteins in the cytoplasm as well as the nucleus.…”

Section: Condensin I Is Located Within the Cytoplasm And Nuclei Durinmentioning

confidence: 57%

The Arabidopsis condensin CAP-D subunits arrange interphase chromatin

Municio

Antosz

Grasser

et al. 2019

Preprint

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Condensins are best known for their role in shaping chromosomes. However, other functions as organizing interphase chromatin and transcriptional control have been reported in yeasts and animals. Yeasts encode one condensin complex, while higher eukaryotes have two of them (condensin I and II). Both, condensin I and II, are conserved in Arabidopsis thaliana, but so far little is known about their function. Here we show that the A. thaliana CAP-D2 (condensin I) and CAP-D3 (condensin II) subunits are highly expressed in mitotically active tissues. In silico and pull-down experiments indicate that both CAP-D proteins interact with the other condensin I and II subunits. Our data suggest that the expression, localization and composition of the condensin complexes in A. thaliana are similar as in other higher eukaryotes. Previous experiments showed that the lack of A. thaliana CAP-D3 leads to centromere association during interphase. To study the function of CAP-D3 in chromatin organization more in detail we compared the nuclear distribution of rDNA, of centromeric chromocenters and of different epigenetic marks, as well as the nuclear size between wild-type and cap-d3 mutants. In these mutants an association of heterochromatic sequences occurs, but nuclear size and the general methylation and acetylation patterns remain unchanged. In addition, transcriptome analyses revealed a moderate influence of CAP-D3 on general transcription, but a stronger one on transcription of stress-related genes. We propose a model for the CAP-D3 function during interphase, where CAP-D3 localizes in euchromatin loops to stiff them, and consequently separates centromeric regions and 45S rDNA repeats.

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“…Percentage of cells with BLM fibers were scored and plotted. Line profiles across the fibers in the cells were analysed using ImageJ as described before [44]. …”

Section: Methodsmentioning

confidence: 99%

Loss of RMI2 Increases Genome Instability and Causes a Bloom-Like Syndrome

et al. 2016

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Bloom syndrome is a recessive human genetic disorder with features of genome instability, growth deficiency and predisposition to cancer. The only known causative gene is the BLM helicase that is a member of a protein complex along with topoisomerase III alpha, RMI1 and 2, which maintains replication fork stability and dissolves double Holliday junctions to prevent genome instability. Here we report the identification of a second gene, RMI2, that is deleted in affected siblings with Bloom-like features. Cells from homozygous individuals exhibit elevated rates of sister chromatid exchange, anaphase DNA bridges and micronuclei. Similar genome and chromosome instability phenotypes are observed in independently derived RMI2 knockout cells. In both patient and knockout cell lines reduced localisation of BLM to ultra fine DNA bridges and FANCD2 at foci linking bridges are observed. Overall, loss of RMI2 produces a partially active BLM complex with mild features of Bloom syndrome.

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Condensin I and II behaviour in interphase nuclei and cells undergoing premature chromosome condensation

Cited by 31 publications

References 80 publications

Mitotic chromosomes fold by condensin-dependent helical winding of chromatin loop arrays

Mitotic chromosomes fold by condensin-dependent helical winding of chromatin loop arrays

The Arabidopsis condensin CAP-D subunits arrange interphase chromatin

Loss of RMI2 Increases Genome Instability and Causes a Bloom-Like Syndrome

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