Time-ordered and flexible motor sequences in C.elegans are generated by combining an excitatory feedforward coupling and mutual inhibitions between neurons in different functional modules.

The flexible escape behavior exhibited by C. elegans in response to threats relies on a combination of feedback and feedforward circuits.

NODAL/Activin-induced SMAD2 binding directly drives remodeling of both open and closed chromatin and does not directly correlate with temporal patterns of gene expression upon prolonged signaling.

A geneome-scale shRNA screen identifies five genes whose suppression promotes cell death upon PI3K inhibition both in vitro and in vivo, thus suggesting potential combination therapies involving PI3K inhibition.

Supporting cells in the cochlea change their shape in response to purinergic receptor activation, which influences hair cell excitability by altering potassium redistribution in the extracellular space.

Digital NF-κB signaling achieves orthogonal control over the probability of activation (percentage of activated cells) and dynamic response heterogeneity in the population via the area and shape of the input profile.

Cells must acquire multiple viral spacer sequences to neutralize mutant escaper phages and form colonies during the CRISPR-Cas immune response.

Activity in the midbrain responds to unexpected changes in outcome identity (i.e. sensory prediction error) but does not scale with perceptual distance between expected and receipt reward.

Ire1's RNase specificity and its cleavage sites coordination shape the evolutionary specialization of the unfolded protein response.

Cutaneous papillomaviruses potentially escape humoral immune response by synthesizing an alternative major capsid protein isoform during the initial course of infection that is unable to induce neutralizing antibodies.