This week’s articles identify a mutation in the acetylcholine receptor that protects poison frogs from the neurotoxin that they produce; explain a key difference between neurons from Parkinson’s patients and those from mouse models of the disease; and review the intermolecular interactions that drive the formation of membraneless intracellular compartments.
MOLECULAR EVOLUTION
Poison frogs resist their own chemical defense
Tarvin et al. showed that poison frogs have evolved mutations in nicotinic acetylcholine receptor genes that confer toxin resistance.
NEUROSCIENCE
Human-derived neurons provide the answers
Burbulla et al. found that the mitochondrial oxidant stress cascade is linked to lysosomal dysfunction in human, but not mouse, dopaminergic Parkinson’s disease neurons.
CELLULAR BIOPHYSICS
Phase separation and cellular organization
Shin and Brangwynne review membraneless cellular assemblies that are important for the segregation of normal cellular function.
