Normal sleep bouts are not essential for C. elegans survival and FoxO is important for compensatory changes in sleep

Additional file 6: Decreased lag-2 function does not slow vulval development. The progeny of wild type and lag-2(q420) animals raised at 25.5 °C were selected at the L4 stage, prior to lethargus entry. Vulval eversion was scored after 3 h; the percentage of animals completing vulval eversion was recorded. Significance was assessed by student’s two-tailed t-test p value < 0.5; error bars represents SEM from 3 trials. Total number of animals: wild type n = 45 and lag-2(q420) n = 42

Homeostasis in C. elegans sleep is characterized by two behaviorally and genetically distinct mechanisms

Biological homeostasis invokes modulatory responses aimed at stabilizing internal conditions. Using tunable photo- and mechano-stimulation, we identified two distinct categories of homeostatic responses during the sleep-like state of Caenorhabditis elegans (lethargus). In the presence of weak or no stimuli, extended motion caused a subsequent extension of quiescence. The neuropeptide Y receptor homolog, NPR-1, and an inhibitory neuropeptide known to activate it, FLP-18, were required for this process. In the presence of strong stimuli, the correlations between motion and quiescence were disrupted for several minutes but homeostasis manifested as an overall elevation of the time spent in quiescence. This response to strong stimuli required the function of the DAF-16/FOXO transcription factor in neurons, but not that of NPR-1. Conversely, response to weak stimuli did not require the function of DAF-16/FOXO. These findings suggest that routine homeostatic stabilization of sleep may be distinct from homeostatic compensation following a strong disturbance. DOI: http://dx.doi.org/10.7554/eLife.04380.00

Male mating behaviour: The importance of waiting

No abstrac

Distinct unfolded protein responses mitigate or mediate effects of nonlethal deprivation of C. elegans sleep in different tissues

Abstract Background Disrupting sleep during development leads to lasting deficits in chordates and arthropods. To address lasting impacts of sleep deprivation in Caenorhabditis elegans, we established a nonlethal deprivation protocol. Results Deprivation triggered protective insulin-like signaling and two unfolded protein responses (UPRs): the mitochondrial (UPRmt) and the endoplasmic reticulum (UPRER) responses. While the latter is known to be triggered by sleep deprivation in rodent and insect brains, the former was not strongly associated with sleep deprivation previously. We show that deprivation results in a feeding defect when the UPRmt is deficient and in UPRER-dependent germ cell apoptosis. In addition, when the UPRER is deficient, deprivation causes excess twitching in vulval muscles, mirroring a trend caused by loss of egg-laying command neurons. Conclusions These data show that nonlethal deprivation of C. elegans sleep causes proteotoxic stress. Unless mitigated, distinct types of deprivation-induced proteotoxicity can lead to anatomically and genetically separable lasting defects. The relative importance of different UPRs post-deprivation likely reflects functional, developmental, and genetic differences between the respective tissues and circuits

Homeostasis in <i>C. elegans</i> sleep is characterized by two behaviorally and genetically distinct mechanisms

Biological homeostasis invokes modulatory responses aimed at stabilizing internal conditions. Using tunable photo- and mechano-stimulation, we identified two distinct categories of homeostatic responses during the sleep-like state of Caenorhabditis elegans (lethargus). In the presence of weak or no stimuli, extended motion caused a subsequent extension of quiescence. The neuropeptide Y receptor homolog, NPR-1, and an inhibitory neuropeptide known to activate it, FLP-18, were required for this process. In the presence of strong stimuli, the correlations between motion and quiescence were disrupted for several minutes but homeostasis manifested as an overall elevation of the time spent in quiescence. This response to strong stimuli required the function of the DAF-16/FOXO transcription factor in neurons, but not that of NPR-1. Conversely, response to weak stimuli did not require the function of DAF-16/FOXO. These findings suggest that routine homeostatic stabilization of sleep may be distinct from homeostatic compensation following a strong disturbance

MOESM2 of Normal sleep bouts are not essential for C. elegans survival and FoxO is important for compensatory changes in sleep

Additional file 2: daf-16 is not required for hypertonic stress resistance in osm-7; osm-11 animals. Hypertonic stress resistance was examined in young adult animals moved to 500mM NaCl NGM plates for 10 min. osm-7(tm2256) and osm-11(rt142) are complete loss of function alleles for Notch DOS family co-ligands. daf-16(mu86) is a partial loss of function allele. Loss of Notch DOS co-ligands results in resistance to hypertonic stress, based on inability to move, spontaneously or upon prodding, after 10 min on 500mM NaCl NGM plates. Partial loss of daf-16 function does not alter hypertonic resistance in these animals. n = 40 animals for all genotypes

MOESM7 of Normal sleep bouts are not essential for C. elegans survival and FoxO is important for compensatory changes in sleep

Additional file 7: Increased lag-2 expression in adults induces anachronistic sleep bouts. Animals carrying hsp::empty, hsp::lag-2 cDNA transgenes, or wild type animals were heat shocked for 1.5 h at 34 °C. After heat shock, animals were allowed to recover at 20 °C for an additional 1 h to recover from stress-induced quiescence (shown in first set of columns). Sleep was scored for all genotypes within 15 min, based on the absence of feeding and movement. Inappropriate sleep in adult animals expressing hsp::lag-2cDNA transgene was reversible, disappearing by 2 h post-heat shock. For all genotypes, n = 40 animals; error bars represent the SEM from 2 independent trials

CRIUS:Undergraduate Research Journal 2014

Volume 2 Number 1 Fall 2014Volume 2 Number 1 of the CRIUS. This journal includes the research of undergraduate students as part of Research & Creative Endeavor SymposiumASU Undergraduate Research Initiativ