Genetic variation in a biogenic amines receptor underlies a means of gain control for nonassociative learning and hence an important form of attention that is the basis for tradeoffs in foraging in a social collective.

Non-invasive disinhibition of the oculomotor system shows that ongoing preparatory activity in the superior colliculus has movement-generating potential and need not rise to threshold in order to produce a saccade.

The conditional reduction of glutaminase in mouse dopamine neurons selectively attenuates glutamate cotransmission at phasic frequencies, revealing the role of dopamine neuron glutamate cotransmission in the attribution of motivational salience.

A gaseous signaling molecule hydrogen sulfide stimulates mitochondrial bioenergetics, maintains glutathione redox poise, and suppresses ROS to subvert viral rebound in latently infected CD4⁺ T cells from HIV subjects.

Analysis of HIV integration sites from induced and non-induced latently infected populations reveals the role of genomic localization and chromatin context in the fate of HIV-1 infection and the reversal of viral latency.

The combination of statistical inference and perturbation experiments reveals that trans-generational inheritance of cell size and cell-cycle speed, coupled through a minimum-size checkpoint, shapes paradoxical cell-cycle correlations in lineage trees.

Inactivation of KAP1 by mTOR-mediated phosphorylation releases human cytomegalovirus from latency, and has the potential to be used as a therapy to purge the virus from transplant organs.

Tgfb3 inhibits Muller glial cell reprogramming and drives Muller cell quiescence in the injured zebrafish retina, thereby inhibiting retina regeneration.

Herpes simplex virus reactivates from a latent infection when neurons become hyperexcitable in response to an inflammatory cytokine known to be released during fever and stress.

CRISPR genome editing technology can efficiently introduce mutations into lytic and latent HSV genomes to block lytic replication and reactivation of latent herpes simplex virus genome though differential mechanisms.