Human gut bacteria alter their metabolism in response to each other's presence, which causes their community dynamics to deviate from predictions that are based on mono-culture data.
Epithelia exhibit size-dependent growth dynamics caused by a decoupling between boundary and bulk cellular dynamics that enable robust expansion and drive cell cycling, collective migration, and tissue-spanning vortices.
Genetic analysis of a CLN4 Drosophila model suggests that the disease-causing alleles act as dominant gain of function mutations that cause CSPα oligomerization and impair secretory and prelysosomal trafficking.
A regulatory circuit that localizes to the synaptonemal complex, a liquid crystalline compartment between chromosomes, ensures crossing-over while limiting the number of crossovers between homologous chromosomes during meiosis.
N-chlorination, a reversible, oxidative modification, turns plasma proteins into holdase-like chaperones, potent activators of immune cells and pro-survival factors for phagocytic immune cells.
