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Time-restricted feeding (TRF) has recently gained interest as a potential anti-ageing treatment for organisms from  Drosophila  to humans 1 – 5 . TRF restricts food intake to specific hours of the day. Because TRF controls the timing of feeding, rather than nutrient or caloric content, TRF has been hypothesized to depend on circadian-regulated functions; the underlying molecular mechanisms of its effects remain unclear. Here, to exploit the genetic tools and well-characterized ageing markers of Drosophila , we developed an intermittent TRF (iTRF) dietary regimen that robustly extended fly lifespan and delayed the onset of ageing markers in the muscles and gut. We found that iTRF enhanced circadian-regulated transcription and that iTRF-mediated lifespan extension required both circadian regulation and autophagy, a conserved longevity pathway. Night-specific induction of autophagy was both necessary and sufficient to extend lifespan on an ad libitum diet and also prevented further iTRF-mediated lifespan extension. By contrast, day-specific induction of autophagy did not extend lifespan. Thus, these results identify circadian-regulated autophagy as a critical contributor to iTRF-mediated health benefits in Drosophila . Because both circadian regulation and autophagy are highly conserved processes in human ageing, this work highlights the possibility that behavioural or pharmaceutical interventions that stimulate circadian-regulated autophagy might provide people with similar health benefits, such as delayed ageing and lifespan extension. Circadian-regulated autophagy contributes to the health benefits of intermittent time-restricted feeding in Drosophila .

Group 3 innate lymphoid cells (ILC3s) are major regulators of inflammation, infection, microbiota composition and metabolism 1 . ILC3s and neuronal cells have been shown to interact at discrete mucosal locations to steer mucosal defence 2 , 3 . Nevertheless, it is unclear whether neuroimmune circuits operate at an organismal level, integrating extrinsic environmental signals to orchestrate ILC3 responses. Here we show that light-entrained and brain-tuned circadian circuits regulate enteric ILC3s, intestinal homeostasis, gut defence and host lipid metabolism in mice. We found that enteric ILC3s display circadian expression of clock genes and ILC3-related transcription factors. ILC3-autonomous ablation of the circadian regulator Arntl led to disrupted gut ILC3 homeostasis, impaired epithelial reactivity, a deregulated microbiome, increased susceptibility to bowel infection and disrupted lipid metabolism. Loss of ILC3-intrinsic Arntl shaped the gut ‘postcode receptors’ of ILC3s. Strikingly, light–dark cycles, feeding rhythms and microbial cues differentially regulated ILC3 clocks, with light signals being the major entraining cues of ILC3s. Accordingly, surgically or genetically induced deregulation of brain rhythmicity led to disrupted circadian ILC3 oscillations, a deregulated microbiome and altered lipid metabolism. Our work reveals a circadian circuitry that translates environmental light cues into enteric ILC3s, shaping intestinal health, metabolism and organismal homeostasis. Circadian circuits, entrained by light and tuned by the brain, regulate intestinal group 3 innate lymphoid cells in mice, along with epithelial reactivity, microbiome composition and lipid metabolism.

Daily changes in light and food availability are major time cues that influence circadian timing 1 . However, little is known about the circuits that integrate these time cues to drive a coherent circadian output 1 – 3 . Here we investigate whether retinal inputs modulate entrainment to nonphotic cues such as time-restricted feeding. Photic information is relayed to the suprachiasmatic nucleus (SCN)—the central circadian pacemaker—and the intergeniculate leaflet (IGL) through intrinsically photosensitive retinal ganglion cells (ipRGCs) 4 . We show that adult mice that lack ipRGCs from the early postnatal stages have impaired entrainment to time-restricted feeding, whereas ablation of ipRGCs at later stages had no effect. Innervation of ipRGCs at early postnatal stages influences IGL neurons that express neuropeptide Y (NPY) (hereafter, IGL NPY neurons), guiding the assembly of a functional IGL NPY –SCN circuit. Moreover, silencing IGL NPY neurons in adult mice mimicked the deficits that were induced by ablation of ipRGCs in the early postnatal stages, and acute inhibition of IGL NPY terminals in the SCN decreased food-anticipatory activity. Thus, innervation of ipRGCs in the early postnatal period tunes the IGL NPY –SCN circuit to allow entrainment to time-restricted feeding. Ablating retinal input at early postnatal stages—but not later time points—impaired entrainment to time-restricted feeding in adult mice, as did silencing intergeniculate-leaflet neurons that express neuropeptide Y and project to the central pacemaker

Environmental enrichment increases adult hippocampal neurogenesis and alters hippocampal-dependent behavior in rodents. To investigate a causal link between these two observations, we analyzed the effect of enrichment on spatial learning and anxiety-like behavior while blocking adult hippocampal neurogenesis. We report that environmental enrichment alters behavior in mice regardless of their hippocampal neurogenic capability, providing evidence that the newborn cells do not mediate these effects of enrichment.

The global increase in the prevalence of obesity and metabolic disorders coincides with the increase of exposure to light at night (LAN) and shift work. Circadian regulation of energy homeostasis is controlled by an endogenous biological clock that is synchronized by light information. To promote optimal adaptive functioning, the circadian clock prepares individuals for predictable events such as food availability and sleep, and disruption of clock function causes circadian and metabolic disturbances. To determine whether a causal relationship exists between nighttime light exposure and obesity, we examined the effects of LAN on body mass in male mice. Mice housed in either bright (LL) or dim (DM) LAN have significantly increased body mass and reduced glucose tolerance compared with mice in a standard (LD) light/dark cycle, despite equivalent levels of caloric intake and total daily activity output. Furthermore, the timing of food consumption by DM and LL mice differs from that in LD mice. Nocturnal rodents typically eat substantially more food at night; however, DM mice consume 55.5% of their food during the light phase, as compared with 36.5% in LD mice. Restricting food consumption to the active phase in DM mice prevents body mass gain. These results suggest that low levels of light at night disrupt the timing of food intake and other metabolic signals, leading to excess weight gain. These data are relevant to the coincidence between increasing use of light at night and obesity in humans.

Background: Worldwide overweight and obesity rates are on the rise, with about 1 900 billion adults being defined as overweight and about 600 million adults being defined as obese by the World Health Organization (WHO). Increasing exposure to artificial light-at-night (ALAN) may influence body mass, by suppression of melatonin production and disruption of daily rhythms, resulting in physiological or behavioral changes in the human body, and may thus become a driving force behind worldwide overweight and obesity pandemic. Methods: We analyzed most recent satellite images of night time illumination, available from the US Defense Meteorological Satellite Program (DMSP), combining them with country-level data on female and male overweight and obesity prevalence rates, reported by the WHO. The study aims to identify and measure the strength of association between ALAN and country-wide overweight and obesity rates, controlling for per capita GDP, level of urbanization, birth rate, food consumption and regional differences. Results: ALAN emerged as a statistically significant and positive predictor of overweight and obesity ( t >1.97; P <0.05), helping to explain, together with other factors, about 70% of the observed variation of overweight and obesity prevalence rates among females and males in more than 80 countries worldwide. Regional differences in the strength of association between ALAN and excessive body mass are also noted. Conclusions: This study is the first population-level study that confirms the results of laboratory research and cohort studies in which ALAN was found to be a contributing factor to excessive body mass in humans.

Although soil organisms are essential for ecosystem function, the impacts of radiation on soil biological activity at highly contaminated sites has been relatively poorly studied. In April-May 2016, we conducted the first largescale deployment of bait lamina to estimate soil organism (largely soil invertebrate) feeding activity in situ at study plots in the Chernobyl Exclusion Zone (CEZ). Across our 53 study plots, estimated weighted absorbed dose rates to soil organisms ranged from 0.7 μGy h -1 to 1753 μGy h -1 . There was no significant relationship between soil organism feeding activity and estimated weighted absorbed dose rate. Soil biological activity did show significant relationships with soil moisture content, bulk density (used as a proxy for soil organic matter) and pH. At plots in the Red Forest (an area of coniferous plantation where trees died because of high radiation exposure in 1986) soil biological activity was low compared to plots elsewhere in the CEZ. It is possible that the lower biological activity observed in the Red Forest is a residual consequence of what was in effect an acute high exposure to radiation in 1986.

For plants, the tradeoff between resource investment in defense and increased growth to out-compete neighbors creates an allocation dilemma. How plants resolve this dilemma, at the mechanistic level, is unclear. We found that Arabidopsis plants produced an attenuated defense phenotype under conditions of crowding and when exposed to far-red (FR) radiation, a light signal that plants use to detect the proximity of neighbors via the photoreceptor phytochrome. This phenotype was detectable through standard bioassays that measured the growth of Spodoptera frugiperda caterpillars. Two possible explanations for the effect of FR are: (i) a simple by-product of the diversion of resources to competition, and (ii) a specific effect of phytochrome on defense signaling. The first possibility was ruled out by the fact that the auxin-deficient sav3 mutant, which fails to induce growth responses to FR, still responded to FR with an attenuated defense phenotype. In support of the second hypothesis, we found that phytochrome inactivation by FR caused a strong reduction of plant sensitivity to jasmonates, which are key regulators of plant immunity. The effects of FR on jasmonate sensitivity were restricted to certain elements of the pathway. Supporting the idea that the FR effects on jasmonate signaling are functionally significant, we found that FR failed to increase tissue quality in jar1, a mutant impaired in jasmonate response. We conclude that the plant modulates its investment in defense as a function of the perceived risk of competition, and that this modulation is effected by phytochrome via selective desensitization to jasmonates.

Biodiversity is negatively affected by light pollution, caused by artificial light at night (ALAN). Light-emitting diodes facilitate new lighting technologies to mediate the negative effects of ALAN, such as dynamic ALAN where light intensity can be adjusted to traffic density. Organisms living in highly light-polluted areas may show adaptations to mitigate the negative effects of ALAN. In a split-brood rearing experiment, larvae of two moth species ( Ochropleura plecta and Agrotis exclamationis ) originating from low-medium and high-medium skyglow populations were grown under either continuous ALAN, dynamic ALAN or control-dark conditions. We tested for ALAN effects on larval mortality, feeding behaviour, development and body mass, and whether effects depended on skyglow levels in the population of origin. Contrary to previous studies, we found either no or positive effects of ALAN on larval development, with similar or stronger effects of dynamic ALAN compared to continuous ALAN. For A. exclamationis , we showed evidence for faster development, increased growth rate and higher body mass under ALAN. This could reduce larval exposure to parasites and increase fecundity. We found no evidence for evolutionary responses in low-medium or high-medium skyglow larvae. Our results show that ALAN does not affect larval development the same way in all species.

During their evolution, plants have acquired diverse capabilities to sense their environment and modify their growth and development as required. The versatile utilization of solar radiation for photosynthesis as well as a signal to coordinate developmental responses to the environment is an excellent example of such a capability. Specific light quality inputs are converted to developmental outputs mainly through hormonal signalling pathways. Accordingly, extensive interactions between light and the signalling pathways of every known plant hormone have been uncovered in recent years. One such interaction that has received recent attention and forms the focus of this review occurs between light and the signalling pathway of the jasmonate hormone with roles in regulating plant defence and development. Here the recent research that revealed new mechanistic insights into how plants might integrate light and jasmonate signals to modify their growth and development, especially when defending themselves from either pests, pathogens, or encroaching neighbours, is discussed.