Metabolic component depletion in model systems results in life-span extension, which has been difficult to reconcile with human metabolic pathologies. Recently, Rea et al. (2007) have shown that mitochondrial electron transport chain RNAi phenotypes in the worm C. elegans are dose dependent, providing an alternative view of mitochondrial function in longevity and metabolic diseases.
Chordate claudins are core components of tight junctions. By contrast, VAB-9, a nematode four-pass transmembrane protein related to claudins, localizes to adherens junctions and contributes to cell adhesion and actin - plasma membrane association.
In the nematode C.elegans, immobility induced by the anesthetic halothane is coupled to its ability to modulate neuronal resting membrane potential, perhaps through effects on leak channels; a similar anesthetic, isoflurane, appears to work a different way.
FOXO transcription factors promote longevity from worms to mammals, but the mechanisms by which FOXO extends lifespan have remained elusive. In the nematode Caenorhabditis elegans, FOXO is now shown to recruit the nucleosome remodelling complex SWI/SNF to its target genes, which is essential for FOXO to elicit stress resistance and longevity.
Aurora A kinase is a key regulator of cell division, whose functions were attributed to its ability to phosphorylate diverse substrates. Aurora A is now shown to have a kinase-independent role in the regulation of chromatin-mediated microtubule assembly.
The tumor suppressor Rb is known to have its hand in many pots. New findings have added another pot to the mix - cell metabolism. This may lead to a better understanding of Rb mutant phenotypes and Rb's roles in oncogenesis.
Autophagy contributes to lipid catabolism through direct mobilization and breakdown of cellular lipid stores. Two recent studies reveal the regulatory mechanisms activated by cells during starvation to ensure that the cellular compartments involved in autophagic lipid catabolism are ready to receive, process and use these lipids. The regulators represent attractive therapeutic targets to help fight lipid-excess-associated diseases.
The small GTPase Arf1 that is classically required for the budding of COPI-coated vesicles from the Golgi membrane is now proposed to have novel and conserved roles in the morphological and functional maintenance of mitochondria: It functionally localizes to ER/mitochondria contact sites; it allows for the recruitment of a degradation machinery to mitochondria to remove toxic mitofusin/Fzo1 clusters; and it allows the extension of autophagy sequestration membranes needed for mitophagy to clear damaged mitochondria.