Modulation of the energy barrier for membrane fusion is a common mechanism by which sensors in the synapse produce supralinear calcium dependence of vesicle release and short-term synaptic potentiation.
Genetic and electrophysiology experiments provide the first direct evidence that protein kinase C is a calcium-sensing protein in post-tetanic potentiation, a form of synaptic plasticity that supports short-term memory.
Synaptotagmin-7 acts synergistically with synaptotagmin-1 by placing vesicles close to the plasma membrane within reach of the SNARE/Munc13-complex, supporting their priming and setting the stage for fast and slow fusion.
Kinesin-4 KIF21B promotes rapid reorientation of the microtubule network during formation of immunological synapse in T cells by acting as a pausing and catastrophe-inducing factor that keeps microtubules short.
Quantifiable bioenergetic parameters, determined from extracellular flux analyses, are distinct between macrophages infected with Mycobacteriumtuberculosis or vaccine strain M. bovis BCG, enabling assessment of future vaccine and drug efficacy.