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The detrimental effects of nuclear factor-kappa B (NF-κB) signalling in cancer cells lacking the oestrogen receptor have now become clear, with the demonstration that increased NF-κB levels induce expression of Bcl-2 to both suppress apoptosis and induce epithelial–mesenchymal transitions (EMTs).
Nine inherited neurodegenerative disorders are caused by polyglutamine (polyQ) expansions in diverse proteins. A study now suggests that polyQ-mediated depletion of nonhistone chromatin proteins enhances genotoxic stress induced by the disease protein.
In mammalian cells, DNA double-strand breaks (DSBs) are repaired by the non-homologous end-joining (NHEJ) pathway. A key component of this repair mechanism is the DNA binding protein, Ku. A recent study shows that Par-3, a protein involved in cell polarity and the assembly of tight junctions, interacts with Ku and is involved in NHEJ, suggesting an intriguing new role for Par-3 and links between cell morphology and DNA damage response pathways.
Viral transmission from an infected cell to a target cell has been long appreciated to be more efficient than infection with a cell-free virus. New work using high-resolution, live-cell microscopy techniques provides important insights into the mechanisms underlying the efficiency of retrovirus transmission between cells.
Lymphocyte migration is activated in response to inflammation and largely depends on the modulation of actin dynamics, and remodelling of the cytoskeleton, following cytokine stimulation. A novel pathway modulating inflammatory-cell migration in vivo that involves the unlikeliest of partners, the inflammatory caspase-11 and Aip1 (an activator of cofilin-mediated actin depolymerization), has been identified.
Mitogen-activated protein kinase (MAPK) cascades process myriads of stimuli, generating receptor-specific cellular outcomes. New work exploits emergent mathematics of network inference to reveal distinct feedback designs of the RAF–MEK–ERK cascade induced by two different growth factors. The study shows that response specificity can arise from differential signal-induced wiring of overlapping protein networks.
Although the molecular machinery controlling aging has been well studied in lower organisms, it is unclear whether these mechanisms are conserved in mammals. A recent study supports a role for an evolutionarily conserved transcriptional pathway in maintaining the unlimited lifespan of haematopoietic stem cells.
Despite being largely a post-mitotic tissue, adult skeletal muscle exhibits a remarkable capacity for regeneration. A new study has shown that cells derived from mural cells (pericytes) from blood vessels in postnatal human skeletal muscle contribute to robust skeletal muscle regeneration after intra-arterial delivery into a dystrophic mouse model.
The microtubule associated protein tau is involved in the neuropathology of Alzheimer's disease, however, the mechanistic basis for the involvement of tau is unclear. New evidence indicates that tau may mediate neurotoxicity by altering the organization and dynamics of the actin cytoskeleton.
The transcription factor GATA-3 is necessary for the formation of a mammary gland and the maintenance of mammary-cell differentiation. The loss of GATA-3 function in a fully formed mammary gland generates oestrogen receptor-negative, proliferating cells that lack expression of myoepithelial markers. Cells with similar characteristics in breast cancer are associated with poor prognosis.
In proliferating cells, the SCFSkp2ubiquitin ligase targets the CDK inhibitor p27 for proteolysis. A study now shows that the tumour suppressor pRb promotes the APC/CCdh1–mediated degradation of Skp2, resulting in the accumulation of p27.
New studies reveal the dynamic accumulation of phosphatidylinositol (3,4,5) trisphosphate (PtdIns(3,4,5)P3) at the leading edge of primary neutrophils during chemotaxis. They also demonstrate that SHIP1, rather than phosphatase and tensin homologue (PTEN), is responsible for the degradation and localization of this lipid in neutrophils and shed light on the role of PtdIns(3,4,5)P3 in directional sensing.
Bone morphogenetic proteins (BMPs) shape vertebrate limbs and define digits by inducing programmed cell death in interdigital tissues. Recent findings show that Drosophila legs are also sculpted by programmed cell death. In this case, rather than the absolute activity of BMP, it is the sharp discontinuity of BMP signalling that is required for forming the leg joint.
In eukaryotes, condensing chromosomal DNA into heterochromatin is important for gene silencing and proper chromosome segregation. A recent study suggests a function for heterochromatin in protecting highly repeated genes and satellite DNA against excision caused by recombination or by joining of free DNA ends following DNA damage.
Each round of DNA replication results in the erosion of telomeres, the ends of linear chromosomes. Telomerase counteracts telomere shortening by synthesizing new DNA sequences in a time period restricted to late S a d G2 cell-cycle phases, even though the enzyme is active throughout the cell cycle. A recent study directly implicates cyclin dependent kinase (Cdk1) in the regulation of telomere elongation during the cell cycle.
