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Stat3 has been shown to regulate lysosome membrane permeabilization and cell death in vivo during post-lactation mammary gland involution. It is now revealed that Stat3 induces lysosome membrane permeabilization by causing phagocytosis of milk fat globules, which destabilize the lysosome membrane leading to leakage of cathepsin proteases.
Despite the importance of cyclins and cyclin-dependent kinases (Cdks) in the control of cell division, the physiological role of many of these regulators remains unknown. Cyclin C and its associated kinases Cdk3, Cdk8 and Cdk19 are now shown to function as tumour suppressors in haematopoietic malignancies by inhibiting the Notch1 pathway.
Payre and colleagues identify a gene, GstE14, needed for production of the insect steroid hormone ecdysone and find that this hormone acts through Pri peptides to control the timing of differentiation events.
Parrinello and colleagues show that direct interactions with endothelial cells in the subventricular zone maintain the quiescence and identity of neural stem cells, through a process involving both Notch- and Ephrin-mediated signalling pathways.
Lysosomal membrane permeabilization releases cathepsins to promote cell death and mammary gland involution. Sargeant et al. report that Stat3-driven phagocytic uptake of fatty acids in milk triglycerides permeabilizes lysosomes to induce cell death.
Murphy and colleagues generate an inhibitor of the lipid kinase VPS34, which they use to uncover autophagy substrates. One of their targets, NCOA4, regulates iron homeostasis by binding ferritin heavy chain-1 and targeting ferritin to autolysosomes.
Through gene knockout experiments, Sicinski and colleagues reveal a role for cyclin C as a haploinsufficient tumour suppressor in T-cell acute lymphoblastic leukaemia, acting through phosphorylation of intracellular Notch1, mediating its degradation.
Lu and colleagues report that ASPP2 induces mesenchymal–epithelial transition and inhibits cancer cell invasion and metastasis by preventing the β-catenin-mediated upregulation of ZEB1.
Weinberg and colleagues report that monocytes and macrophages interact with stem-like human mammary epithelial cells to create a breast cancer stem cell niche.
Furuta and colleagues report that single dynein molecules are kept in an autoinhibited state through the stacking of their two head domains. This autoinhibition is relieved when dynein molecules assemble together on cargo.
