UC Berkeley

The correct function of organisms ranging from bacteria to humans critically depends on the cells’ ability to rapidly change its metabolism through dedicated signaling cascades that transduce signals present in the surrounding environment. Two examples of these signaling cascades: mechanistic target of rapamycin complex 1 (mTORC1) and cAMP-dependent protein kinase A (PKA) work in tangent with cellular processes like autophagy to maintain cellular homeostasis. The two-way regulation between mTORC1 and autophagy is clear but the relationship between autophagy and PKA is more complex. Here I will focus on this complex interaction and propose a model where autophagy is regulating the PKA holoenzyme but also becomes a signaling scaffold for AKAP11-bound PKA. Furthermore, I also talk about the implications of our findings in the context of schizophrenia and bipolar disorder.