Abstract:Environmental temperature acclimation is essential to animal survival, yet thermoregulation mechanisms remain poorly understood. We demonstrate cold tolerance in as regulated by paired ADL chemosensory neurons via Ca-dependent endoribonuclease (EndoU) ENDU-2. Loss of ENDU-2 function results in life span, brood size, and synaptic remodeling abnormalities in addition to enhanced cold tolerance. Enzymatic ENDU-2 defects localized in the ADL and certain muscle cells led to increased cold tolerance in mutants. Ca i… Show more
“…1 b) 5 , 11 – 14 . For example, ADL can respond to temperature stimuli, as indicated by an increased Ca 2+ concentration in ADL upon warming 12 , which leads to changes of cold tolerance and temperature acclimatisation. Figure 1 Thermosensory neurons regulate cold tolerance and temperature acclimatisation in C. elegans .…”
mentioning
confidence: 99%
“…TRPV channels OSM-9, OCR-1, and OCR-2 act in temperature sensation by ADL (Fig. 1 b) 12 , 15 . Thermal-dependent Ca 2+ concentration changes in ADL upon warming stimuli in osm-9 ocr-2; ocr-1 triple mutant animals were decreased compared with wild-type ADL 12 .…”
mentioning
confidence: 99%
“…1 b) 12 , 15 . Thermal-dependent Ca 2+ concentration changes in ADL upon warming stimuli in osm-9 ocr-2; ocr-1 triple mutant animals were decreased compared with wild-type ADL 12 . Cultivation of OSM-9/OCR-1/OCR-2 mutants at 25 °C resulted in abnormal temperature acclimatisation and decreased ADL neural activity in response to temperature stimuli, suggesting that TRP channels are necessary for ADL temperature signalling for temperature acclimatisation 12 , 15 .…”
Caenorhabditis elegans (C. elegans) exhibits cold tolerance and temperature acclimatisation regulated by a small number of head sensory neurons, such as the ADL temperature-sensing neurons that express three transient receptor potential vanilloid (TRPV) channel subunits, OSM-9, OCR-2, and OCR-1. Here, we show that an OSM-9/OCR-2 regulates temperature acclimatisation and acts as an accessorial warmth-sensing receptor in ADL neurons. Caenorhabditis elegans TRPV channel mutants showed abnormal temperature acclimatisation. Ectopic expression of OSM-9 and OCR-2 in non-warming-responsive gustatory neurons in C. elegans and Xenopus oocytes revealed that OSM-9 and OCR-2 cooperatively responded to warming; however, neither TRPV subunit alone was responsive to warming. A warming-induced OSM-9/OCR-2-mediated current was detectable in Xenopus oocytes, yet ADL in osm-9 ocr-2 double mutant responds to warming; therefore, an OSM-9/OCR-2 TRPV channel and as yet unidentified temperature receptor might coordinate transmission of temperature signalling in ADL temperature-sensing neurons. This study demonstrates direct sensation of warming by TRPV channels in C. elegans.
“…1 b) 5 , 11 – 14 . For example, ADL can respond to temperature stimuli, as indicated by an increased Ca 2+ concentration in ADL upon warming 12 , which leads to changes of cold tolerance and temperature acclimatisation. Figure 1 Thermosensory neurons regulate cold tolerance and temperature acclimatisation in C. elegans .…”
mentioning
confidence: 99%
“…TRPV channels OSM-9, OCR-1, and OCR-2 act in temperature sensation by ADL (Fig. 1 b) 12 , 15 . Thermal-dependent Ca 2+ concentration changes in ADL upon warming stimuli in osm-9 ocr-2; ocr-1 triple mutant animals were decreased compared with wild-type ADL 12 .…”
mentioning
confidence: 99%
“…1 b) 12 , 15 . Thermal-dependent Ca 2+ concentration changes in ADL upon warming stimuli in osm-9 ocr-2; ocr-1 triple mutant animals were decreased compared with wild-type ADL 12 . Cultivation of OSM-9/OCR-1/OCR-2 mutants at 25 °C resulted in abnormal temperature acclimatisation and decreased ADL neural activity in response to temperature stimuli, suggesting that TRP channels are necessary for ADL temperature signalling for temperature acclimatisation 12 , 15 .…”
Caenorhabditis elegans (C. elegans) exhibits cold tolerance and temperature acclimatisation regulated by a small number of head sensory neurons, such as the ADL temperature-sensing neurons that express three transient receptor potential vanilloid (TRPV) channel subunits, OSM-9, OCR-2, and OCR-1. Here, we show that an OSM-9/OCR-2 regulates temperature acclimatisation and acts as an accessorial warmth-sensing receptor in ADL neurons. Caenorhabditis elegans TRPV channel mutants showed abnormal temperature acclimatisation. Ectopic expression of OSM-9 and OCR-2 in non-warming-responsive gustatory neurons in C. elegans and Xenopus oocytes revealed that OSM-9 and OCR-2 cooperatively responded to warming; however, neither TRPV subunit alone was responsive to warming. A warming-induced OSM-9/OCR-2-mediated current was detectable in Xenopus oocytes, yet ADL in osm-9 ocr-2 double mutant responds to warming; therefore, an OSM-9/OCR-2 TRPV channel and as yet unidentified temperature receptor might coordinate transmission of temperature signalling in ADL temperature-sensing neurons. This study demonstrates direct sensation of warming by TRPV channels in C. elegans.
“…Among the genes that displayed the largest upregulation were T07F10.1 (anp-1) a poorly-characterized aminopeptidase ortholog of mammalian endoplasmic reticulum aminopeptidase (ERAP1), and ERAP2 (endoplasmic reticulum aminopeptidase 2), that by analogy to its role in other nematodes, could play roles in digestion, metabolite excretion, neuropeptide processing and/or osmotic regulation (Davey and Sommerville 1974), fbxb-19, K10G4.10 and fbxa-103 three of the 326 predicted F-box containing proteins in C. elegans (Kipreos and Pagano 2000) and genes predicted to encode proteins that were either transcription factors, or had DNA binding activity. Among the downregulated genes we found those that encode proteins directly involved in metabolism such as F42A10.9, an enzyme predicted to be involved in the breakdown of crosslinked proteins, gfat-2 a glucosamine-fructose-6-phosphate aminotransferase predicted to catalyze the first step in the hexosamine pathway (Ghosh et al 2014), lys-10 a lysozyme involved in longevity (Samuelson et al 2007), endu-2, an endonuclease important for stress tolerance (Ujisawa et al 2018;Battisti et al 2017), acs-2 involved in fatty acid metabolism (Liang et al 2010;Nomura et al 2010), and asp-8, predicted to have endopeptidase activity. Thus, it appeared that the loss of 5-HT caused an overall increase in gene expression within the animal, as well as significantly downregulated genes that could alter metabolism.…”
Section: The Chronic Lack Of Serotonin Causes a Net Increase In Gene mentioning
Serotonin (5-hydroxytryptamine, 5-HT), is a phylogenetically ancient molecule best characterized as a neurotransmitter that modulates multiple aspects of mood and social cognition. The roles that 5-HT plays in normal and abnormal behavior are not fully understood but have been posited to be due to its common function as a ‘defense signal’. However, 5-HT levels also systemically impact cell physiology, modulating cell division, migration, apoptosis, mitochondrial biogenesis, cellular metabolism and differentiation. Whether these diverse cellular effects of 5-HT also share a common basis is unclear. C. elegans provides an ideal system to interrogate the systemic effects of 5-HT, since lacking a blood-brain barrier, 5-HT synthesized and released by neurons permeates the organism to modulate neuronal as well as non-neuronal cells throughout the body. Here we used RNA-Seq to characterize the systemic changes in gene expression that occur in C. elegans upon altering 5-HT levels, and compared the transcriptomes to published datasets. We find that an acute increase in 5-HT is accompanied by a global decrease in gene expression levels, upregulation of genes involved in stress pathways, changes that significantly correlate with the published transcriptomes of animals that have activated defense and immune responses, and an increase in levels of phosphorylated eukaryotic initiation factor, eIF2α. In 5-HT deficient animals lacking tryptophan hydroxylase (tph-1(mg280) II) there is a net increase in gene expression, with an overrepresentation of genes related to development and chromatin. Surprisingly, the transcriptomes of animals with acute increases in 5-HT levels, and 5-HT deficiency do not overlap with transcriptomes of mutants with whom they share striking physiological resemblance. These studies are the first to catalog systemic transcriptome changes that occur upon alterations in 5-HT levels. They further show that in C. elegans changes in gene expression upon altering 5-HT levels, and changes in physiology, are not directly correlated.
“…In addition to sensing harsh touch, PVD acts as a thermosensor activated by cold temperatures 53 . Cold-shock has been previously studied as a stressor for C. elegans [53][54][55][56][57][58][59][60][61][62][63][64] . Robinson et alidentified that animals can survive short (4 hrs.)…”
Section: Acute Cold-shock Induces Neurodegeneration In Pvd Neuronmentioning
Access to quantitative information is crucial to obtain a deeper understanding of biological systems. In addition to being low-throughput, traditional image-based analysis is mostly limited to error-prone qualitative or semi-quantitative assessment of phenotypes, particularly for complex subcellular morphologies. In this work, we apply deep learning to perform quantitative imagebased analysis of complex neurodegeneration patterns exhibited by the PVD neuron in C. elegans. We apply a Convolutional Neural Network algorithm (Mask R-CNN) to identify neurodegenerative sub-cellular protrusions that appear after cold-shock or as a result of aging. A multiparametric phenotypic profile captures the unique morphological changes induced by each perturbation. We identify that acute cold-shock-induced neurodegeneration is reversible and depends on rearing temperature, and importantly, that aging and cold-shock induce distinct neuronal beading patterns.
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