Search

NDC80 complex (NDC80C) is composed of four subunits (SPC24, SPC25, NDC80, and NUF2) and is vital for kinetochore–microtubule (KT–MT) attachment during mitosis. Paradoxically, NDC80C also functions in the activation of the spindle-assembly checkpoint (SAC). This raises an interesting question regarding how mitosis is regulated when NDC80C levels are compromised. Using a degron-mediated depletion system, we found that acute silencing of SPC24 triggered a transient mitotic arrest followed by mitotic slippage. SPC24-deficient cells were unable to sustain SAC activation despite the loss of KT–MT interaction. Intriguingly, our results revealed that other subunits of the NDC80C were co-downregulated with SPC24 at a posttranslational level. Silencing any individual subunit of NDC80C likewise reduced the expression of the entire complex. We found that the SPC24–SPC25 and NDC80–NUF2 subcomplexes could be individually stabilized using ectopically expressed subunits. The synergism of SPC24 downregulation with drugs that promote either mitotic arrest or mitotic slippage further underscored the dual roles of NDC80C in KT–MT interaction and SAC maintenance. The tight coordinated regulation of NDC80C subunits suggests that targeting individual subunits could disrupt mitotic progression and provide new avenues for therapeutic intervention.

In order to advance the development of quantum emitter-based devices, it is essential to enhance light-matter interactions through coupling between semiconductor quantum dots with high quality factor resonators. Here, efficient tuning of the emission properties of HgTe quantum dots in the infrared spectral region is demonstrated by coupling them to a plasmonic metasurface that supports bound states in the continuum. The plasmonic metasurface, composed of an array of gold nanobumps, is fabricated using single-step direct laser printing, opening up new opportunities for creating exclusive 3D plasmonic nanostructures and advanced photonic devices in the infrared region. A 12-fold enhancement of the photoluminescence in the 900–1700 nm range is observed under optimal coupling conditions. By tuning the geometry of the plasmonic arrays, controllable shaping of the emission spectra is achieved, selectively enhancing specific wavelength ranges across the emission spectrum. The observed enhancement and shaping of the emission are attributed to the Purcell effect, as corroborated by systematic measurements of radiative lifetimes and optical simulations based on the numerical solution of Maxwell's equations. Moreover, coupling of the HgTe photoluminescence to high quality factor modes of the metasurface improves emission directivity, concentrating output within an ≈20° angle. © 2023 Wiley-VCH GmbH.

Whole-genome duplication (WGD) is one of the most common genomic abnormalities in cancers. WGD can provide a source of redundant genes to buffer the deleterious effect of somatic alterations and facilitate clonal evolution in cancer cells. The extra DNA and centrosome burden after WGD is associated with an elevation of genome instability. Causes of genome instability are multifaceted and occur throughout the cell cycle. Among these are DNA damage caused by the abortive mitosis that initially triggers tetraploidization, replication stress and DNA damage associated with an enlarged genome, and chromosomal instability during the subsequent mitosis in the presence of extra centrosomes and altered spindle morphology. Here, we chronicle the events after WGD, from tetraploidization instigated by abortive mitosis including mitotic slippage and cytokinesis failure to the replication of the tetraploid genome, and finally, to the mitosis in the presence of supernumerary centrosomes. A recurring theme is the ability of some cancer cells to overcome the obstacles in place for preventing WGD. The underlying mechanisms range from the attenuation of the p53-dependent G(1) checkpoint to enabling pseudobipolar spindle formation via the clustering of supernumerary centrosomes. These survival tactics and the resulting genome instability confer a subset of polyploid cancer cells proliferative advantage over their diploid counterparts and the development of therapeutic resistance.