Mathematical models with experimental validation show that chloride transporters in the cell membrane, and not negatively charged impermeant molecules, generate the driving force used by GABA receptors to silence neurons.
Electrophysiological and simulation approaches show that a chloride-related longer relaxation of the inhibitory synaptic events partially compensates the early defect in the chloride homeostasis detected in fetal SOD spinal motoneurons.
Systematic analyses of DNA replication machinery components in human cells reveal a requirement of MCM-dependent de novo loading or mobilization of cohesin at replication forks in establishing sister-chromatid cohesion.
Sister chromatid cohesion is established during replication by two independent pathways operating in parallel, one converts chromosomal cohesin into cohesive structures while the other loads cohesin onto nascent DNAs.
The effects of chloride homeostasis can explain diverse responses of basal ganglia output neurons to putatively inhibitory inputs and may tune these neurons' synchrony, oscillations and behavior in decision-making scenarios.
E3 ubiquitin ligase Bre1-induced H2B monoubiquitination is epigenetically important for recruiting replication factor Mcm10 and cohesion establishment factors Ctf4, Ctf18 and Eco1 to early replication origins to establish sister chromatid cohesion.