Volume 9 Issue 8, August 2007

Permeabilization of the mitochondria usually leads to caspase activation and apoptosis. In the absence of caspase activation, these same mitochondrial changes can also lead to cell death. A recent study suggests that when good mitochondria go bad, the activation of both glycolysis and autophagy may permit cellular survival.

Last year it was reported that a cocktail of four transcription factors — encoded by Oct4, Sox2, Myc and Klf4 — can partly reprogramme mouse somatic cells to an embryonic state, a process that reawakens silenced segments of the genome and restores pluripotency to the somatic cell nucleus. Three groups have now modified this method to generate fully reprogrammed cells that closely resemble embryonic stem cells.

PIM protein kinases have been known for some time as oncogenes that promote lymphomagenesis together with MYC (c-Myc). It is now reported that PIM1 is a coactivator of MYC, and it phosphorylates serine 10 of histone H3 at MYC target genes. These results may shed new mechanistic light on how PIM1 cooperates with MYC in tumorigenesis.

Membrane microdomains are widely postulated to regulate cell signalling, especially at the plasma membrane. Despite intense study, how this occurs remains largely unknown. New work now suggests that for MAP (mitogen-activated protein) kinase signalling, microdomains containing Ras nanoclusters contribute to the fidelity of signal transduction by acting as digital switches.

The molecular mechanisms through which the epidermal growth factor receptor (EGFR) promotes normal cell migration and carcinoma invasion are incompletely understood. A new study reveals that EGFR induces a switch in expression from tensin to its endogenous inhibitor cten (C-terminal tensin-like protein), alleviating integrin linkage to the cytoskeleton. Analysis of clinical samples suggests that this may be important for breast cancer invasion.

A new study of the zebrafish intestine has uncovered a transcriptional hierarchy controlling lumen formation and proposes a model for how transcellular and paracellular transport synergize to ensure that only a single lumen is produced.