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Pan et al. found that actomyosin-II–driven reversible beading underpins the resilience of central axons to mild mechanical stress by suppressing the propagation and firing of injurious Ca2+ waves. Boosting actomyosin-II activity alleviates axon degeneration in mice with traumatic brain injury.

In budding yeast, the growth of the daughter bud is required for mitotic progression. Analysis of signals that control bud growth suggests that the mitotic exit network (MEN) ensures that mitotic exit occurs only when an appropriate amount of bud growth has occurred.

The microtubule-associated cues that underlie the position and traffic of endosomes are poorly understood. Robinson et al. report that endosomes with multivesicular body and late endosome markers localize preferentially to microtubules coated with septins, which promote maturation of CD63 enriched endosomes by hindering their mobility.

Barnaba, Broabent et al. develop K-FOCUS for high-throughput analysis of autophagy foci in human cells and demonstrate that glucose starvation downregulates autophagy via AMP-activated protein kinase, which prevents phagophore tethering to donor membranes to inhibit autophagosome maturation.

The authors discovered histone H3K36me2, which is believed to be enriched in potentially active genomic regions, is also located in transcriptionally inactive regions called heterochromatin in some cell types. The detailed molecular mechanism of its heterochromatin targeting is now revealed.

Ruehle, Li, and colleagues identify the conserved Poc1 protein to be a triplet microtubule inner junction protein that seals triplet microtubules and supports basal body integrity. Poc1 promotes proximal and core structures that interconnect triplet microtubules and enable forces from beating cilia to be resisted.

In this study, the authors investigate how cells regulate proteasome content in response to catabolic stimuli in vivo. During cellular adaptation to accelerated proteolysis, muscle cells boost proteasome levels by inducing proteasome subunit genes and assembly chaperones in a two-phase transcriptional program that is controlled by multiple transcription factors.

The findings reveal how calcium regulates migrasome formation and propose a sequential interaction model involving Syt1 and Tetraspanins in the formation and stabilization of migrasomes. The research uncovers a pivotal step that facilitates the transition from tension-induced swelling to the establishment of a stable migrasome.

Binucleated polyploid hepatocytes are common in the mammalian liver, but it is unclear how they arise in humans. Darmasaputra et al. investigate how binucleated cells arise in human fetal–derived hepatocyte organoids, demonstrating a late cytokinetic regression during the endomitosis M phase.

Report

Bagdadi et al. show that, although usually considered inactive, GDP-bound tubulin polymerizes into remarkably stable microtubules. These results reveal that microtubules possess an intrinsic capacity for stability, independent of accessory proteins. This finding provides novel mechanisms to revisit microtubule dynamics.

Chong et al. show that chromosomes biorient and correct errors with varying efficiencies. Chromosome size and the spindle forces that scale with size determine error correction efficiency such that elevated tension at kinetochores on long chromosomes allows premature stabilization of non-bioriented attachments, delaying their alignment.

In human cells, the S-phase-promoting kinase CDC7 exists in two alternative complexes: CDC7-DBF4 or CDC7-DRF1. Here, Göder et al. show that while CDC7’s essential function can be supported by both subunits, DBF4 is the primary mediator of CDC7 activity during DNA replication.

Perspective

Nabi and colleagues discuss supervision paradigms for biological discovery from super-resolution microscopy to enable AI-accelerated exploration of the nanoscale architecture of subcellular macromolecules and organelles.

Huna et al. provide insights into the shifting perception of cellular senescence: from a mere cell proliferation arrest to a reinforcement or change of cell identity.

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