New reconstruction methods are used to create a publicly available dense reconstruction of the neurons and chemical synapses of central brain of Drosophila, with analysis of its graph properties.

When conscious visual perception changes, the observer's pupils simultaneously signal the accompanying change in visual cortical representation, and specific neuromodulatory activity that helps translate the altered visual experience into behavior.

Comparision of current and fluorescent kinetics from P2X7 receptor mutants labeled with the fluorescent amino acid ANAP suggests that the characteristic P2X7 current facilitation involves changes in channel gating rather than interactions or conformational changes of its intracellular ballast domain.

The bacterial AAA+ chaperone ClpL recognizes aggregated proteins via multiple contacts of its unique N-terminal domain and refolds them with high efficiency providing superior heat resistance.

QuantEv is a fully automatic and semi-parametric method that allows quantitative analysis of the spatio-temporal distribution of complex molecular trafficking objects at the scale of the whole cell.

In vitro assays using Xenopus egg extracts provide evidence that mitosis-specific loading of condensin I is accelerated by phosphorylation of the N-terminal tail of its kleisin subunit.

A single protein catalyzes site-specific DNA recombination upon blue-light illumination.

A combined approach of genome sequencing and fluctuation assays shows that antibiotic pressure does not induce adaptive mutations in Mycobacterium smegmatis, supporting drug resistance as a consequence of phenotypic tolerance.

In vivo and in vitro elongation factor-RNA interaction data provide a missing link in understanding how processive elongation complexes are formed on active genes and disassembled at the end of genes.

Central damage and sensory deprivation caused by noise-induced hearing loss in the pre-symptomatic Alzheimer's disease (AD) phase can compromise auditory cortex-hippocampal circuitry, targeting common pathogenetic pathways, thereby accelerating onset and progression of AD phenotype.