Germ cell ablation delays C. elegans aging, in part, because unconsumed fat triggers activation of the detoxification factor SKN-1/Nrf, which is regulated by lipid signals and maintains lipid homeostasis.
The mechanism underlying Shprintzen–Goldberg syndrome is solved and reveals that missense mutations in the transcriptional repressor SKI abolish ligand-induced SKI degradation, which results in attenuation of TGF-β transcriptional responses.
Brassinosteroids signal through a pathway involving GSK3-like kinases and the WER-GL3/EGL3-TTG1 transcription factor complex to determine the fate of cells in the root epidermis.
Serotonin neurons in chronically isolated mice become less responsive to excitatory stimulation, but inhibiting a distinctive calcium-activated potassium channel can restore both neuronal activity and behavior.
Skd3 (human ClpB) is a potent ATP-dependent mitochondrial protein disaggregase that is activated by the rhomboid protease, PARL, and inactivated by MGCA7-linked mutations.
Microtubule binding by the Spindle and Kinetochore Associated (Ska) complex concentrates protein phosphatase 1 at metaphase kinetochores to overcome the spindle checkpoint thus driving anaphase onset and mitotic exit.
Binding of two macromolecular complexes allows kinetochores to capture force produced by the depolymerising ends of microtubules, allowing chromosomes to be transmitted from a mother cell to its two daughters.
Intersectin counterparts in yeast recruit WASP and WIP to endocytic sites to establish a robust multivalent SH3 domain-PRM interaction network which gives actin assembly onset a switch-like behavior in vivo.