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Aneuploidy, which results from chromosome mis-segregation, is a hallmark of cancer, but it can also inhibit tumorigenesis. Recent studies on the short- and long-term consequences of aneuploidy, which are caused by gene-specific effects and a stereotypic aneuploidy stress response, provide insights into this contradictory role in tumorigenesis.
Repressive histone Lys methyltransferases (KMTs) mediate gene silencing by methylating histone H3 Lys 9 (H3K9), H3K27 and H4K20. Progress has been made in our understanding of the biochemical and functional properties of KMTs, the mechanisms of their recruitment to chromatin and the interplay between them.
Inhibition of mTOR by rapamycin attenuates the translation of interleukin-1α, thus reducing the secretion of inflammatory cytokines by senescent cells.
Autophagy serves to degrade proteins during starvation. Recent progress has illuminated how, during starvation and nutrient repletion, autophagy can mobilize diverse cellular energy and nutrient stores, such as lipids, carbohydrates and iron, to salvage key metabolites that sustain and facilitate core anabolic functions.
Transcription-blocking DNA lesions displace spliceosomes from chromatin and activate a non-canonical ataxia-telangiectasia mutated signalling pathway that modulates splicing.
Recent findings revealed that DNA–protein crosslinks (DPCs) in yeast and Xenopus laevis are repaired by a dedicated, protease-based DNA-repair pathway. Mutations in the putative human homologue of a DPC protease result in premature ageing and cancer predisposition.
Actomyosin-mediated contractility generates mechanical stress in animal cells and underlies muscle contraction, cell migration, cell division and tissue morphogenesis. Insight into the mechanics of actomyosin arrays that lack sarcomeric organization has revealed novel modes of force transmission and shown that diverse mechanical behaviours can arise from common molecular components.
The function of p53 as a tumour suppressor has been attributed to its ability to promote cell death or permanently inhibit cell proliferation. However, p53 can also contribute to cell survival by regulating various metabolic pathways to allow cells to adapt to mild metabolic stresses.
