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Based on cryo-EM structures, here the authors propose three models for how the inner kinetochore and CENP-A nucleosomes are organized on repetitive alpha-satellite sequences, providing insights into the higher-order architecture of human centromeres.

Chromosomes bind microtubules (MT) from opposite spindle poles and the generated tension stabilizes kinetochore-MT attachments. Here the authors measure kinetochore forces by engineering two force sensors and propose that kinetochore fibers exert hundreds of pNs of force to bioriented kinetochores.

Kinetochores are large structures composed of hundreds of proteins that assemble onto centromeric DNA to form a microtubule-binding site that is essential for proper chromosomal segregation. The structure of budding-yeast kinetochore particles is now studied by EM and electron tomography, revealing a large central hub surrounded by multiple globular domains, and multiple attachment sites for microtubules.

Here, the authors determine the structure of the human outer kinetochore KMN network complex, showing that it forms an extended and rigid rod-like structure and that it exists in an auto-inhibited state which can be relieved by phosphorylation.

Tension stabilizes properly attached microtubules to kinetochores during chromosome segregation, and lack of tension leads to release. Here the authors show that tension directly suppresses Aurora B kinase mediated destabilization of reconstituted kinetochore-microtubule attachments, likely ensuring accurate chromosome segregation.

The kinetochore is a multi-complex structure that helps attach chromosomes to spindle microtubules, ensuring accurate chromosome segregation during cell division. Kinetochores are thought to be evolutionarily conserved, but which components are conserved is unclear. Here, the authors report that some members of the fungal phylum of Basidomycota lack many conventional kinetochore linker proteins. Instead, they possess a human Ki67-like protein that bridges the outer part of the kinetochore to centromere DNA, which may compensate for the loss of a conventional linker.

Thousands of centromeres were identified and tracked across two major fungal clades, showing that new centromeres spread progressively and that the kinetochore acts as a filter to determine which new centromere variants are tolerated.

Chromosomes must move to the spindle center for efficient cell division. Here, the authors describe a kinetochore-based molecular switch involving CENP-E and Aurora kinases that controls the timing of chromosome movement by regulating end-on attachment stability.

CENcyclopedia reveals the dynamic architecture of kinetochore proteins throughout the cell cycle, providing a foundational framework for understanding accurate chromosome partitioning during cell division.

In general, the kinetochore position and the sister-chromatid cohesion site are spatially linked. Here, the authors find a meiosis-specific distal cohesion site decoupled from the kinetochore in Peromyscus mice, breaking the dogma.

The spindle assembly checkpoint protects cells from chromosome missegregation. Here, the authors use sophisticated biochemical reconstitutions to address how kinetochores, the microtubule-binding structures of chromosomes, regulate this checkpoint.

The spindle assembly factor HURP and the kinesin motor Kif18A are known to regulate mitotic spindle dynamics. Here, the authors show that HURP concentration on kinetochore-fibers modulates the landing and motility of Kif18A, providing a mechanism for microtubule length control.

Mitotic chromosomes recruit multiple microtubule-directed activities to ensure their faithful segregation. Using an approach where only one major activity is present, the authors reveal sufficiency of kinetochore dynein for chromosome biorientation.

The γ-tubulin ring complex (γ-TuRC) nucleates microtubules. The nuclear pore subcomplex Nup107-160 is found to interact and cooperate with γ-TuRC to nucleate microtubules at kinetochores, thereby promoting spindle assembly.

Helsen et al. use experimental evolution and chromosome engineering to probe the link between karyotype changes and the cell division machinery. They conclude that spindle organization dictates the available trajectories for karyotype evolution.

Long noncoding RNA SAM (Sugt1 associated muscle) is upregulated in the proliferating myoblast cells. Here the authors investigate SAM knockout mice and suggest that SAM binds and stabilizes Sugt1, a co-chaperone protein that regulates kinetochore assembly.

Metaphase chromosomes oscillate while attached to growing and shrinking microtubules. Here, the authors show that an α-tubulin detyrosination gradient on kinetochore microtubules fine-tunes load-bearing attachments during chromosome oscillations.

It is unknown how the kinetochore fibrous corona is disassembled. Here, the authors reveal that Aurora A and B kinases-mediated phosphorylation activates CENP-E, which is essential to prevent the premature removal of corona proteins by dynein.

The exact function of kinetochore proteins in meiosis remains unclear. Using live imaging of C. elegans oocytes, the authors systematically study the contribution of each kinetochore sub-complex and describe a push-pull mechanism that confers robustness to chromosome segregation.

The cryoEM structures of a single protofilament of FtsZ from Klebsiella pneumoniae (KpFtsZ) in a polymerization-preferred conformation are presented and of a double-helical tube of the FtsZ–monobody complex that shows two parallel protofilaments.

During cell division, chromosome alignment is engendered by connection of microtubules to kinetochores, coordinated by Aurora B and PLK1. Here, the authors show that the RSF1-PLK1 axis creates an activating phosphorylation on T236 in the GT motif of Aurora B and this is indispensable for Aurora B activation.

Chromosome instability frequently occurs due to issues with chromosome-microtubule attachments. Here the authors show that the Astrin-PP1 and Cyclin-B-CDK1 pathways counteract each other to protect chromosome-microtubule attachments independent of biorientation.

Sissoko et al. show that CENP-T local concentration regulates its ability to recruit the outer kinetochore, which may restrict complete kinetochore formation to regions with higher-order inner kinetochore assemblies.

During cell division, kinetochores anchor chromosomes to spindle microtubules. Here, the authors report a comprehensive structure–function analysis of the kinetochore’s main microtubule receptor, the KMN network, shedding new light on its organization.

During cell division, tetraploidy can drive chromosomal instability (CIN) via supernumerary centrosomes, but it is unclear if this is the only route to CIN. Here the authors show that, in early mouse embryos, tetraploidy can drive chromosomal instability by altering microtubule dynamics and attachment.

During cell division, it is currently unclear how kinetochores transit from lateral microtubule attachment to durable association to dynamic microtubule plus ends. Here, using in vitro reconstitution and computer modeling, the authors provide biophysical mechanism for microtubule end-conversion driven by two kinetochore components, CENP-E and Ndc80 complex

Centromeres are the sites of kinetochore and inner centromere formation, which can be epigenetically regulated. Here, the authors reveal a role for the lymphocyte specific helicase LSH/Hells associated with pericentric heterochromatin formation in centromere stability and chromosome segregation at meiotic kinetochores.

Zhou et al. design protein-based artificial kinetochore constructs as decoys to prevent premature chromosomal separation in aged oocytes. These constructs compete with chromosomal kinetochores, reducing excessive bipolar microtubule pulling forces.

Kinetochores assemble on centromeres via histone H3 variant CENP-A and low levels of centromere transcripts (cenRNAs). Here the authors show the Rio1 kinase limits cenRNA production by reducing RNAPII accessibility and promotes cenRNA degradation by the 5’− 3’exoribonuclease Rat1.

The Aurora kinases orchestrate chromosome segregation and cell division. Zeeshan et al. studied divergent Plasmodium ARK2 and EB1 using live cell imaging, proteomics and functional genetics. These are critical components for atypical spindle dynamics during transmission stages.

The spindle assembly checkpoint protects against premature chromosome segregation during mitosis but it is not known whether microtubule attachment to the kinetochore, or force generated from this interaction, is being monitored. Here the authors uncouple these processes and show that microtubule attachment is sufficient to satisfy the checkpoint.

The spindle assembly checkpoint prevents mitotic progression when chromosomes are not properly attached to the mitotic spindle. Here Tauchman et al.show that stable microtubule attachment to the kinetochore, and not tension generated from this interaction, is sufficient to silence the checkpoint.

Sister chromatid cohesion during meiosis II (MII), maintained by securin-mediated inhibition of separase, is reduced in aged mouse oocytes. Here the authors show that, in MII oocytes, securin levels are reduced by increased destruction by the anaphase promoting complex/cyclosome.

The deposition of histone H3 variant CENP-A bound with histone H4 is a key feature designating the centromere region of a chromosome. Here the authors show acetylation on residues K5 and K12 in histone H4, mediated by the RbAp46/48-Hat1 complex, is required for deposition of CENP-A-H4 into centromeres.

The oligomeric Dam1 complex mediates microtubule attachment to kinetochores during mitosis; however, the significance of its oligomeric structure remains unclear. Umbreit et al. show that Dam1 oligomerization is required for microtubules to form attachments that are robust against tension.

Centromeres are centrochromatin domains with CENP-A and H3 nucleosomes carrying transcription-associated modifications. Here the authors target synthetic modules to the centromeres to show that transcription plus histone modifications are required for CENP-A assembly and centrochromatin maintenance.

The long elusive mammalian meiosis-specific kinetochore factor has been identified in mice; MEIKIN—which plays an equivalent role to the yeast proteins Spo13 and Moa1—ensures mono-orientation, protects sister chromatid cohesion and recruits the kinase PLK1 to the kinetochores.

Kinetochores must interact with both polymerizing (straight) and depolymerizing (curved) microtubules to ensure correct mitotic chromosome segregation. Abad et al. reveal how this flexibility is achieved through structural characterization of the interactions between microtubules and the kinetochore protein Ska1.

PP2A-B56 regulates the stability of kinetochore-microtubule attachments by dephosphorylating several kinetochore proteins. Porter et al. identify Bod1 as a specific inhibitor of PP2A-B56 phosphatase activity and show that this activity is required for proper chromosome alignment during mitosis.

Mitotic exit is controlled by a cell division checkpoint that prevents premature degradation of cyclin B by the anaphase-promoting complex. Saurinet al. show that Aurora B directly regulates timely establishment of this checkpoint by facilitating activation of Mps1 kinase at unattached kinetochores.

The BubR1/Bub3 complex regulates chromosome segregation to enable proper kinetochore-microtubule interactions and is also required for the spindle assembly checkpoint. Here the authors show that two distinct pools of BubR1/Bub3 exist at kinetochores to support both known functions of BubR1/Bub3.

Kinetochores assemble on centromeric DNA and link centromeres to spindle microtubules, thus allowing proper segregation during mitosis. The kinetochore subunit Ndc10 makes contacts with centromeric DNA elements, which are now directly observed in a crystal structure. Along with biochemical analyses, the work indicates that Ndc10 functions as a central organizing hub to assemble the inner kinetochore.

Polo-like kinase 1 (PLK1) regulates the spindle assembly checkpoint and is recruited to prometaphase kinetochores. Kim et al.show that the condensin subunit NCAPG2 is required for stable interaction of PLK1 with kinetochores and for proper chromosome segregation.

The kinetochores contain multiple protein interaction networks. Takenoshita et al. analyzed the complicated networks using the genetic method and revealed that two copies of Ndc80 complexes on CENP-T are sufficient for kinetochore functions.

Chromosome segregation is essential to avoid aneuploidy, yet in mammalian oocytes it progressively fails in an age-dependent manner. Here the authors identify CENP-V as a microtubule binding and bundling protein crucial to faithful oocyte meiosis, and present Cenp-V−/− oocytes as revealing age-dependent weakening of the spindle assembly checkpoint.

How the chromosome passenger complex (CPC) phosphorylates the kinetochores that can be a micron away to control mitotic events is unknown. Here the authors find that the CPC directly binds microtubules near inner centromeres, which controls its ability to phosphorylate kinetochores independently of tension generated by kinetochore microtubule attachments.

While the biological roles of ubiquitin chains are well studied, little is known about the functions of SUMO polymers. Here, the authors identify poly-SUMOylation substrates and provide evidence that SUMO polymers regulate the accumulation of CCAN subunits at chromatin and centromeres.

The CENP-A chaperone HJURP associates with Mis18α, Mis18β, and M18BP1 to target centromeres and deposit new CENP-A. Here the authors provide evidence that two repeats in human HJURP previously proposed to be functionally distinct are interchangeable and bind concomitantly to the 4:2:2 Mis18α:Mis18β:M18BP1 complex without dissociating it.