Sinking slowly: Diversity in propensity to trust predicts downward trust spirals in small groups.

This paper examines the phenomenon of trust spirals in small groups. Drawing on literature on the spiral reinforcement of trust, we theorize that diversity in propensity to trust has affective and cognitive consequences related to trust (i.e., feelings of frustration and perceptions of low similarity), reducing the level of experienced intragroup trust early in a group's development. Reduced experienced trust then fuels relationship conflict and lowers trust even further over time, ultimately having a negative effect on group performance. These ideas are tested using a sample of MBA student groups surveyed at 3 time periods over 4 months. Results confirm our hypothesis that diversity in propensity to trust is sufficient to trigger a downward trust spiral and poor performance in small groups.

ß-adrenergic signaling inhibits Gq-dependent protein kinase D activation by preventing protein kinase D translocation.

RATIONALE: Both ß-adrenergic receptor (ß-AR) and Gq-coupled receptor (GqR) agonist-driven signaling play key roles in the events, leading up to and during cardiac dysfunction. How these stimuli interact at the level of protein kinase D (PKD), a nodal point in cardiac hypertrophic signaling, remains unclear. OBJECTIVE: To assess the spatiotemporal dynamics of PKD activation in response to ß-AR signaling alone and on coactivation with GqR-agonists. This will test our hypothesis that compartmentalized PKD signaling reconciles disparate findings of PKA facilitation and inhibition of PKD activation. METHODS AND RESULTS: We report on the spatial and temporal profiles of PKD activation using green fluorescent protein-tagged PKD (wildtype or mutant S427E) and targeted fluorescence resonance energy transfer-based biosensors (D-kinase activity reporters) in adult cardiomyocytes. We find that ß-AR/PKA signaling drives local nuclear activation of PKD, without preceding sarcolemmal translocation. We also discover pronounced interference of ß-AR/cAMP/PKA signaling on GqR-induced translocation and activation of PKD throughout the cardiomyocyte. We attribute these effects to direct, PKA-dependent phosphorylation of PKD-S427. We also show that phosphomimetic substitution of S427 likewise impedes GqR-induced PKD translocation and activation. In neonatal myocytes, S427E inhibits GqR-evoked cell growth and expression of hypertrophic markers. Finally, we show altered S427 phosphorylation in transverse aortic constriction-induced hypertrophy. CONCLUSIONS: ß-AR signaling triggers local nuclear signaling and inhibits GqR-mediated PKD activation by preventing its intracellular translocation. PKA-dependent phosphorylation of PKD-S427 fine-tunes the PKD responsiveness to GqR-agonists, serving as a key integration point for ß-adrenergic and Gq-coupled stimuli.

From approach to inhibition: the influence of power on responses to poor performers.

This article examines how relative differences in power affect responses to poor performers in organizations. We predicted that higher power individuals would engage in approach-related behaviors, whereas lower power individuals would be inhibited when responding to poor performers. Results from a scenario study and a field study generally supported this prediction, indicating that power was positively related to training or confronting a poor performer and negatively related to compensating for or rejecting a poor performer. A second scenario study investigated the effect of the interaction of power and emotion on individual responses to poor performers. Results showed that the type of emotion expressed moderated the effect of power on inhibition-related responses. We discuss implications for managing poor performers with relative power differences.