CTCF is essential for proper mitotic spindle structure and anaphase segregation

Chiu, Katherine; Berrada, Yasmin; Eskndir, Nebiyat; Song, Dong; Fong, Claire; Naughton, Sarah; Chen, Tina; Moy, Savanna; Gyurmey, Sarah; James, Liam; Ezeiruaku, Chimere; Capistran, Caroline; Lowey, Daniel; Diwanji, Vedang; Peterson, Samantha J.; Parakh, Harshini R; Burgess, Ayanna R; Probert, Cassandra; Zhu, Annie; Anderson, Bryn; Levi, Nehora; Gerlitz, Gabi; Packard, Mary; Dorfman, Katherine A; Bahiru, Michael Seifu; Stephens, Andrew D.

doi:10.1101/2023.01.09.523293

Cited by 3 publications

(3 citation statements)

References 61 publications

(70 reference statements)

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“…Therefore, a small amount of HpCTCF may exist on mitotic chromosomes and spindles and contribute to sister chromatid segregation. A recent report showed that the CRISPR‐mediated knockdown of CTCF leads to disorganized tri/tetrapolar spindle formation and impairment of anaphase segregation in mouse B16‐F1 cells (Chiu et al, 2023).…”

Section: Discussionmentioning

confidence: 99%

The crucial role of CTCF in mitotic progression during early development of sea urchin

et al. 2023

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CCCTC‐binding factor (CTCF), an insulator protein with 11 zinc fingers, is enriched at the boundaries of topologically associated domains (TADs) in eukaryotic genomes. In this study, we isolated and analyzed the cDNAs encoding HpCTCF, the CTCF homolog in the sea urchin Hemicentrotus pulcherrimus, to investigate its expression patterns and functions during the early development of sea urchin. HpCTCF contains nine zinc fingers corresponding to fingers 2–10 of the vertebrate CTCF. Expression pattern analysis revealed that HpCTCF mRNA was detected at all developmental stages and in the entire embryo. Upon expressing the HpCTCF‐GFP fusion protein in early embryos, we observed its uniform distribution within interphase nuclei. However, during mitosis, it disappeared from the chromosomes and subsequently reassembled on the chromosome during telophase. Moreover, the morpholino‐mediated knockdown of HpCTCF resulted in mitotic arrest during the morula to blastula stage. Most of the arrested chromosomes were not phospholylated at serine 10 of histone H3, indicating that mitosis was arrested at the telophase by HpCTCF depletion. Furthermore, impaired sister chromatid segregation was observed using time‐lapse imaging of HpCTCF‐knockdown embryos. Thus, HpCTCF is essential for mitotic progression during the early development of sea urchins, especially during the telophase‐to‐interphase transition. However, the normal development of pluteus larvae in CRISPR‐mediated HpCTCF‐knockout embryos suggests that disruption of zygotic HpCTCF expression has little effect on embryonic and larval development.

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Section: Discussionmentioning

confidence: 99%

The crucial role of CTCF in mitotic progression during early development of sea urchin

et al. 2023

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“…Therefore, a small amount of HpCTCF may exist on mitotic chromosomes and spindles, and contribute to sister chromatid segregation. A recent report showed that the CRISPR-mediated knockdown of CTCF leads to disorganized tri/tetrapolar spindle formation and impairment of anaphase segregation in mouse B16-F1 cells (Chiu et al, 2023).…”

Section: Discussionmentioning

confidence: 99%

The Crucial Role of CTCF in Mitotic Progression during Early Development of Sea Urchin

Watanabe

Fujita

Okamoto

et al. 2023

Preprint

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CCCTC-binding factor (CTCF), an insulator protein with 11 zinc fingers, is enriched at the boundaries of topologically associated domains (TADs) in eukaryotic genomes. In this study, we isolated and analyzed the cDNAs encoding HpCTCF, the CTCF homolog in the sea urchin Hemicentrotus pulcherrimus, to investigate its expression patterns and functions during early development of sea urchin. HpCTCF contains nine zinc fingers corresponding to fingers 2-10 of the vertebrate CTCF. The expression pattern analysis revealed that HpCTCF mRNA was detected at all developmental stages and in the entire embryo. Upon expressing the HpCTCF-GFP fusion protein in early embryos, we observed its uniform distribution within interphase nuclei. However, during mitosis, it disappeared from the chromosomes and subsequently reassembled on the chromosome during telophase. Moreover, the morpholino-mediated knockdown of HpCTCF resulted in mitotic arrest during the morula-to-blastula stage. Most of the arrested chromosomes were not phospholylated at serine 10 of histone H3, indicating that mitosis was arrested at the telophase by HpCTCF depletion. Furthermore, impaired sister chromatid segregation was observed using time-lapse imaging of HpCTCF-knockdown embryos. Thus, HpCTCF is essential for mitotic progression during the early development of sea urchins, especially during the telophase-to-interphase transition. However, the normal development of pluteus larvae in CRISPR-mediated HpCTCF knockout embryos suggests that disruption of zygotic HpCTCF expression has little effect on embryonic and larval development.

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“…Chromatin, chromatin proteins, and chromatin-related processes directly influence nuclear mechanics and shape. [1–5] Nuclear stability is further maintained by multiple processes, including by the nuclear lamina, a meshwork of type V intermediate filament proteins called lamins. [6] Besides its role in maintaining nuclear stiffness and stability, the lamina plays critical roles in regulating gene expression and DNA replication through chromatin interactions.…”

Section: Introductionmentioning

confidence: 99%

Nuclear blebs are associated with destabilized chromatin packing domains

Pujadas Liwag,

Acosta,

Almassalha

et al. 2024

Preprint

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Disrupted nuclear shape is associated with multiple pathological processes including premature aging disorders, cancer-relevant chromosomal rearrangements, and DNA damage. Nuclear blebs (i.e., herniations of the nuclear envelope) have been induced by (1) nuclear compression, (2) nuclear migration (e.g., cancer metastasis), (3) actin contraction, (4) lamin mutation or depletion, and (5) heterochromatin enzyme inhibition. Recent work has shown that chromatin transformation is a hallmark of bleb formation, but the transformation of higher-order structures in blebs is not well understood. As higher-order chromatin has been shown to assemble into nanoscopic packing domains, we investigated if (1) packing domain organization is altered within nuclear blebs and (2) if alteration in packing domain structure contributed to bleb formation. Using Dual-Partial Wave Spectroscopic microscopy, we show that chromatin packing domains within blebs are transformed both by B-type lamin depletion and the inhibition of heterochromatin enzymes compared to the nuclear body. Pairing these results with single-molecule localization microscopy of constitutive heterochromatin, we show fragmentation of nanoscopic heterochromatin domains within bleb domains. Overall, these findings indicate that translocation into blebs results in a fragmented higher-order chromatin structure.

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CTCF is essential for proper mitotic spindle structure and anaphase segregation

Cited by 3 publications

References 61 publications

The crucial role of CTCF in mitotic progression during early development of sea urchin

The crucial role of CTCF in mitotic progression during early development of sea urchin

The Crucial Role of CTCF in Mitotic Progression during Early Development of Sea Urchin

Nuclear blebs are associated with destabilized chromatin packing domains

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