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Bone remodelling in vertebrates is coordinately regulated by the opposing effects of parathyroid hormone (PTH) and transforming growth factor-beta (TGF-β). PTH couples the processes of bone resorption and formation by enforcing simultaneous internalization of TGF-β type II receptor (TβRII) and PTH type 1 receptor (PTH1R), which attenuates both TGF-β and PTH signalling in vivo.
The p62 protein recognizes toxic cellular waste, which is then scavenged by a sequestration process known as self-eating or autophagy. Lack of autophagy leads to accumulation of p62, which is not good for liver cells, as it induces a cellular stress response that leads to disease.
The microRNA miR-9 is induced by Myc in breast cancer cells where it targets the major epithelial adherens junction protein, E-cadherin. This primes the cancer cells for epithelial–mesenchymal transition (EMT) and also stimulates angiogenesis in tumours.
Recent studies have revealed a prominent role of mitochondrial dysfunction in the development of one of the most common neurodegenerative disorders, Parkinson's disease. The ubiquitin ligase Parkin and the protein kinase PINK1, whose mutations are associated with Parkinson's disease, function in a pathway that links ubiquitylation with selective autophagy of damaged mitochondria.
Separation of sister chromatids at anaphase in metazoan cells requires only the cleavage of the kleisin subunit of centromeric cohesin, but efficient poleward movement of separated sisters requires the associated loss in Cdk1 activity. Activation of the anaphase-promoting complex/cyclosome ensures these events are coordinated.
Adipocytes and scar tissue form during skeletal muscle degeneration. Two new studies reveal that adipocytes and fibroblasts in skeletal muscle derive from a population of bipotent progenitors that reside within muscle, but are not derived from the muscle lineage. These progenitor cells also have a surprising role in stimulating the restoration of muscle mass during regeneration.
Exosomes are endosome-derived membrane vesicles that are key for intercellular communication in the immune system and elsewhere. Rab27A and Rab27B GTPases and two of their cognate effector proteins seem to be needed to drive the physiologically important exosome-release process in certain cell types.
During development, proliferating cells are organized into compartments with boundaries across which cells fail to intermix. Compartment boundaries are often attributed to differential cell–cell adhesion between separate compartments. However, tension generated by actomyosin cables at boundaries can also function as a barrier that prevents cell mixing.
Cdk2 has been shown to have an unanticipated role in suppressing Myc-induced senescence. This has implications for how c-Myc overcomes failsafe mechanisms to induce tumorigenesis and suggests that the inhibition of Cdk2 may have therapeutic efficacy in the treatment of cancer.
