Stu-71air-2 is a C. elegans aurora homologue essential for chromosome segregation during embryonic and post-embryonic development

Chromatin condition is crucial for the cells to respond to their environment. In C. elegans, post-embryonic development is accompanied by the exit of progenitor cells from quiescence in response to food. The chromatin protein LET-418/Mi2 is required for this transition in development indicating that proper chromatin structure in cells of the freshly hatched larvae is important to respond to food. However, the identity of the tissue or cells where LET-418/Mi2 is required, as well as the developmental signals that it is modulating have not been elucidated. By restoring the activity of LET-418/Mi2 in specific tissues, we demonstrate that its activity in the intestine and the hypodermis is able to promote in a cell non-autonomous manner the exit of blast cells from quiescence and further development. Furthermore, we identify the IIS (insulin/insulin-like growth factor signaling) pathway to be one of the signaling pathways that is conveying LET-418/Mi2 cell non-autonomous effect on development.

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Unique and redundant functions of C. elegans HP1 proteins in post-embryonic development

Developmental Biology ◽

10.1016/j.ydbio.2006.06.039 ◽

2006 ◽

Vol 298 (1) ◽

pp. 176-187 ◽

Cited By ~ 36

Author(s):

Sonia Schott ◽

Vincent Coustham ◽

Thomas Simonet ◽

Cecile Bedet ◽

Francesca Palladino

Keyword(s):

Embryonic Development ◽

C Elegans ◽

Redundant Functions ◽

Hp1 Proteins

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The axial element protein HTP-3 promotes cohesin loading and meiotic axis assembly in C. elegans to implement the meiotic program of chromosome segregation

Genes & Development ◽

10.1101/gad.1808809 ◽

2009 ◽

Vol 23 (15) ◽

pp. 1763-1778 ◽

Cited By ~ 111

Author(s):

A. F. Severson ◽

L. Ling ◽

V. van Zuylen ◽

B. J. Meyer

Keyword(s):

Chromosome Segregation ◽

C Elegans ◽

Axial Element

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Mitotic chromosome condensation requires phosphorylation of the centromeric protein KNL-2 in C. elegans

10.1101/2021.07.01.450752 ◽

2021 ◽

Author(s):

Joanna M Wenda ◽

Reinier F Prosée ◽

Caroline Gabus ◽

Florian A Steiner

Keyword(s):

Chromosome Segregation ◽

Mitotic Chromosome ◽

Chromosome Condensation ◽

Embryonic Lethality ◽

Phosphorylation Sites ◽

C Elegans ◽

Microtubule Attachment ◽

Centromeric Protein ◽

Mitotic Chromosome Condensation

Centromeres are chromosomal regions that serve as sites for kinetochore formation and microtubule attachment, processes that are essential for chromosome segregation during mitosis. Centromeres are almost universally defined by the histone variant CENP-A. In the holocentric nematode C. elegans, CENP-A deposition depends on the loading factor KNL-2. Depletion of either CENP-A or KNL-2 results in defects in centromere maintenance, chromosome condensation and kinetochore formation, leading to chromosome segregation failure. Here, we show that KNL-2 is phosphorylated by CDK-1, and that mutation of three C-terminal phosphorylation sites causes chromosome segregation defects and an increase in embryonic lethality. In strains expressing phosphodeficient KNL-2, CENP-A and kinetochore proteins are properly localised, indicating that the role of KNL-2 in centromere maintenance is not affected. Instead, the mutant embryos exhibit reduced mitotic levels of condensin II on chromosomes and significant chromosome condensation impairment. Our findings separate the functions of KNL-2 in CENP-A loading and chromosome condensation and demonstrate that KNL-2 phosphorylation regulates the cooperation between centromeric regions and the condensation machinery in C. elegans.

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Male meiotic spindle features that efficiently segregate paired and lagging chromosomes

10.1101/737494 ◽

2019 ◽

Author(s):

Gunar Fabig ◽

Robert Kiewisz ◽

Norbert Lindow ◽

James A. Powers ◽

Vanessa Cota ◽

...

Keyword(s):

Chromosome Segregation ◽

Chromosome Pairing ◽

Electron Tomography ◽

Male Meiosis ◽

Meiotic Spindle ◽

Sperm Production ◽

C Elegans ◽

Anaphase Onset ◽

Unpaired Chromosome ◽

Anaphase B

AbstractChromosome segregation during male meiosis is tailored to rapidly generate multitudes of sperm. Little, however, is known about the mechanisms that efficiently segregate chromosomes to produce sperm. Using live imaging in Caenorhabditis elegans, we find that spermatocytes exhibit simultaneous pole-to-chromosome shortening (anaphase A) and pole-to-pole elongation (anaphase B). Electron tomography unexpectedly revealed that spermatocyte anaphase A does not stem from kinetochore microtubule shortening. Instead, movement is driven by changes in distance between chromosomes, microtubules, and centrosomes upon tension release at anaphase onset. We also find that the lagging X chromosome, a distinctive feature of anaphase I in C. elegans males, is due to lack of chromosome pairing. The unpaired chromosome remains tethered to centrosomes by continuously lengthening kinetochore microtubules which are under tension, suggesting a ‘tug of war’ that can reliably resolve chromosome lagging. Overall, we define features that partition both paired and lagging chromosomes for optimal sperm production.

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Condensin DC spreads linearly and bidirectionally from recruitment sites to create loop-anchored TADs in C. elegans

10.1101/2021.03.23.436694 ◽

2021 ◽

Cited By ~ 1

Author(s):

David Sebastian Jimenez ◽

Jun Kim ◽

Bhavana Ragipani ◽

Bo Zhang ◽

Lena Annika Street ◽

...

Keyword(s):

Chromosome Segregation ◽

X Chromosome ◽

Molecular Motors ◽

Sequence Motif ◽

X Chromosomes ◽

C Elegans ◽

Eukaryotic Chromosome ◽

Multiple Copies

AbstractCondensins are molecular motors that compact DNA for chromosome segregation and gene regulation. In vitro experiments have begun to elucidate the mechanics of condensin function but how condensin loading and translocation along DNA controls eukaryotic chromosome structure in vivo remains poorly understood. To address this question, we took advantage of a specialized condensin, which organizes the 3D conformation of X chromosomes to mediate dosage compensation (DC) in C. elegans. Condensin DC is recruited and spreads from a small number of recruitment elements on the X chromosome (rex). We found that ectopic insertion of rex sites on an autosome leads to bidirectional spreading of the complex over hundreds of kilobases. On the X chromosome, strong rex sites contain multiple copies of a 12-bp sequence motif and act as TAD borders. Inserting a strong rex and ectopically recruiting the complex on the X chromosome or an autosome creates a loop-anchored TAD. Unlike the CTCF system, which controls TAD formation by cohesin, direction of the 12-bp motif does not control the specificity of loops. In an X;V fusion chromosome, condensin DC linearly spreads into V and increases 3D DNA contacts, but fails to form TADs in the absence of rex sites. Finally, we provide in vivo evidence for the loop extrusion hypothesis by targeting multiple dCas9-Suntag complexes to an X chromosome repeat region. Consistent with linear translocation along DNA, condensin DC accumulates at the block site. Together, our results support a model whereby strong rex sites act as insulation elements through recruitment and bidirectional spreading of condensin DC molecules and form loop-anchored TADs.

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Cyclin B3 activates the Anaphase-Promoting Complex/Cyclosome in meiosis and mitosis

10.1101/2020.06.05.136291 ◽

2020 ◽

Author(s):

Damien Garrido ◽

Mohammed Bourouh ◽

Éric Bonneil ◽

Pierre Thibault ◽

Andrew Swan ◽

...

Keyword(s):

Embryonic Development ◽

Chromosome Segregation ◽

Ubiquitin Ligase ◽

Anaphase Promoting Complex ◽

Cells In Culture ◽

Cyclin B3 ◽

Mitosis And Meiosis ◽

In Cells

ABSTRACTIn mitosis and meiosis, chromosome segregation is triggered by the Anaphase-Promoting Complex/Cyclosome (APC/C), a multi-subunit ubiquitin ligase that targets proteins for degradation, leading to the separation of chromatids. APC/C activation requires phosphorylation of its APC3 and APC1 subunits, which allows the APC/C to bind its Cdc20 co-activator. The identity of the kinase(s) responsible for APC/C activation in vivo is unclear. Cyclin B3 is required for meiotic anaphase in flies, worms and vertebrates, but whether it activates the APC/C is unclear. We found that Drosophila Cyclin B3 (CycB3) collaborates with PP2A-B55/Tws in embryonic development, indicating that CycB3 also promotes anaphase in mitosis. Moreover, CycB3 promotes APC/C activity and anaphase in cells in culture. We show that CycB3 physically associates with the APC/C, is required for phosphorylation of APC3, and promotes APC/C association with its co-activators. We propose that CycB3-Cdk1 directly phosphorylates the APC/C to activate it in both meiosis and mitosis.

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