Dweck's Social-Cognitive Model of Achievement Motivation in Science.

Dweck's social-cognitive model has long been used as a basis for achievement motivation research. However, few studies have examined the comprehensive model with interactions between perceived ability and achievement goals, and even fewer studies have focused on this model in a science academic context. With a sample of undergraduates (n = 1,036), the relations among mindsets, science academic self-efficacy, achievement goals, and achievement-related outcomes in science were examined. Fixed mindset related to performance goals. Growth mindset related to mastery goals and the number of courses completed. There was a significant indirect effect of growth mindset on interest value via mastery goals. Contrary to Dweck's model, the relation of performance goals to outcomes did not vary as a function of science academic self-efficacy. The findings provide empirical evidence for a more nuanced understanding of Dweck's model. They provide practical insights for how to support undergraduate students who are pursuing science-related career.

Integrated proteomics reveals autophagy landscape and an autophagy receptor controlling PKA-RI complex homeostasis in neurons.

Autophagy is a conserved, catabolic process essential for maintaining cellular homeostasis. Malfunctional autophagy contributes to neurodevelopmental and neurodegenerative diseases. However, the exact role and targets of autophagy in human neurons remain elusive. Here we report a systematic investigation of neuronal autophagy targets through integrated proteomics. Deep proteomic profiling of multiple autophagy-deficient lines of human induced neurons, mouse brains, and brain LC3-interactome reveals roles of neuronal autophagy in targeting proteins of multiple cellular organelles/pathways, including endoplasmic reticulum (ER), mitochondria, endosome, Golgi apparatus, synaptic vesicle (SV) for degradation. By combining phosphoproteomics and functional analysis in human and mouse neurons, we uncovered a function of neuronal autophagy in controlling cAMP-PKA and c-FOS-mediated neuronal activity through selective degradation of the protein kinase A - cAMP-binding regulatory (R)-subunit I (PKA-RI) complex. Lack of AKAP11 causes accumulation of the PKA-RI complex in the soma and neurites, demonstrating a constant clearance of PKA-RI complex through AKAP11-mediated degradation in neurons. Our study thus reveals the landscape of autophagy degradation in human neurons and identifies a physiological function of autophagy in controlling homeostasis of PKA-RI complex and specific PKA activity in neurons.