Dietary E. coli promotes age-dependent chemotaxis decline in C. elegans.

An animal's ability to sense odors declines during aging, and its olfactory drive is tuned by internal states such as satiety. However, whether internal states modulate an age-dependent decline in odor sensation is unknown. To address this issue, we utilized the nematode Caenorhabditis elegans and compared their chemotaxis abilities toward attractive odorants when aged under different dietary conditions. Feeding with the standard laboratory diet, Escherichia coli attenuated the chemotaxis ability toward diacetyl, isoamyl alcohol, and benzaldehyde when aged. On the other hand, feeding with either the lactic acid bacteria Lactobacillus reuteri or food deprivation selectively maintained the chemotaxis ability toward diacetyl. Our results suggest that ingestion of E. coli causes age-dependent chemotaxis decline. The changes in the chemotaxis behavior are attributed to the different expressions of diacetyl receptor odr-10, and the chemotaxis behavior of aged animals under food deprivation is shown to be dependent on daf-16. Our study demonstrates the molecular mechanism of how diet shapes the trajectory of age-dependent decline in chemosensory behaviors.

What happens when the lights are left on? Transcriptomic and phenotypic habituation to light pollution.

Artificial light at night (ALAN) is a ubiquitous pollutant worldwide. Exposure can induce immediate behavioral and physiological changes in animals, sometimes leading to severe health consequences. Nevertheless, many organisms persist in light-polluted environments and may have mechanisms of habituating, reducing responses to repeated exposure over time, but this has yet to be tested experimentally. Here, we tested whether zebra finches (Taeniopygia guttata) can habituate to dim (0.3 lux) ALAN, measuring behavior, physiology (oxidative stress and telomere attrition), and gene expression in a repeated measures design, over 6 months. We present evidence of tolerance to chronic exposure, persistent behavioral responses lasting 8 weeks post-exposure, and attenuation of responses to re-exposure. Oxidative stress decreased under chronic ALAN. Changes in the blood transcriptome revealed unique responses to past exposure and re-exposure. Results demonstrate organismal resilience to chronic stressors and shed light on the capacity of birds to persist in an increasingly light-polluted world.

Dim artificial light at night alters immediate early gene expression throughout the avian brain.

Artificial light at night (ALAN) is a pervasive pollutant that alters physiology and behavior. However, the underlying mechanisms triggering these alterations are unknown, as previous work shows that dim levels of ALAN may have a masking effect, bypassing the central clock. Light stimulates neuronal activity in numerous brain regions which could in turn activate downstream effectors regulating physiological response. In the present study, taking advantage of immediate early gene (IEG) expression as a proxy for neuronal activity, we determined the brain regions activated in response to ALAN. We exposed zebra finches to dim ALAN (1.5 lux) and analyzed 24 regions throughout the brain. We found that the overall expression of two different IEGs, cFos and ZENK, in birds exposed to ALAN were significantly different from birds inactive at night. Additionally, we found that ALAN-exposed birds had significantly different IEG expression from birds inactive at night and active during the day in several brain areas associated with vision, movement, learning and memory, pain processing, and hormone regulation. These results give insight into the mechanistic pathways responding to ALAN that underlie downstream, well-documented behavioral and physiological changes.