Sleep on it, but only if it is difficult:effects of sleep on problem solving

Previous research has shown that performance on problem solving improves over a period of sleep compared to wakefulness. However, these studies have not determined whether sleep is beneficial for problem solving or whether sleep merely mitigates against interference due to an interruption to solution attempts. Sleep-dependent improvements have been described in terms of spreading-activation, which raises the prediction that an effect of sleep should be greater for problems requiring a broader solution search. We presented participants with a set of remote associates tasks that varied in difficulty as a function of the strength of the stimuli-answer associations. After a period of sleep, wake, or no-delay, participants reattempted previously unsolved problems. The sleep group solved more difficult problems than the other groups, but no difference was found for easy problems. We conclude that sleep facilitates problem solving, most likely via spreading activation, but this has its primary effect for harder problem

A truncated isoform of the PP2A B56 subunit promotes cell motility through paxillin phosphorylation

Both F10 and BL6 sublines of B16 mouse melanoma cells are metastatic after intravenous injection, but only BL6 cells are metastatic after subcutaneous injection. Retrotransposon insertion was found to produce an N–terminally truncated form (Δγ1) of the B56γ1 regulatory subunit isoform of protein phosphatase (PP) 2A in BL6 cells, but not in F10 cells. We found an interaction of paxillin with PP2A C and B56γ subunits by co-immunoprecipitation. B56γ1 co-localized with paxillin at focal adhesions, suggesting a role for this isoform in targeting PP2A to paxillin. In this regard, Δγ1 behaved similarly to B56γ1. However, the Δγ1-containing PP2A heterotrimer was insufficient for the dephosphorylation of paxillin. Transfection with Δγ1 enhanced paxillin phosphorylation on serine residues and recruitment into focal adhesions, and cell spreading with an actin network. In addition, Δγ1 rendered F10 cells as highly metastatic as BL6 cells. These results suggest that mutations in PP2A regulatory subunits may cause malignant progression