scholarly journals Activity-dependent regulation of the proapoptotic BH3-only gene egl-1 in a living neuron pair in C. elegans

2019 ◽  
Author(s):  
Jesse Cohn ◽  
Vivek Dwivedi ◽  
Nicole Zarate ◽  
H Robert Horvitz ◽  
Jonathan T Pierce
Keyword(s):  
Nervous System ◽  
Protein Kinase ◽  
Genetic Screening ◽  
Protein Kinase G ◽  
Neuron Pair ◽  
C Elegans ◽  
Cellular Processes ◽  
Epistasis Analysis ◽  
Activity Dependent ◽  
Shed Light

ABSTRACTThe BH3-only family of proteins is key for initiating apoptosis in a variety of contexts, and may also contribute to non-apoptotic cellular processes. Historically, the nematode Caenorhabditis elegans has provided a powerful system for studying and identifying conserved regulators of BH3-only proteins. In C. elegans, the BH3-only protein EGL-1 is expressed during development to cell-autonomously trigger most developmental cell deaths. Here we provide evidence that egl-1 is also transcribed after development in the sensory neuron pair URX without inducing apoptosis. We used genetic screening and epistasis analysis to determine that its transcription is regulated in URX by neuronal activity and/or in parallel by orthologs of Protein Kinase G and the Salt-Inducible Kinase family. Because several BH3-only family proteins are also expressed in the adult nervous system of mammals, we suggest that studying egl-1 expression in URX may shed light on mechanisms that regulate conserved family members in higher organisms.

scholarly journals Repression of an activity-dependent autocrine insulin signal is required for sensory neuron development in C. elegans

2018 ◽  
Author(s):  
Lauren Bayer Horowitz ◽  
Julia P. Brandt ◽  
Niels Ringstad
Keyword(s):  
Nervous System ◽  
System Development ◽  
Nervous System Development ◽  
P38 Map Kinase ◽  
Dependent Manner ◽  
Neuron Development ◽  
C Elegans ◽  
Chemosensory Neuron ◽  
Insulin Receptor Signaling ◽  
Activity Dependent

AbstractNervous system development is instructed both by genetic programs and activity-dependent refinement of gene expression and connectivity. How these mechanisms are integrated remains poorly understood. Here, we report that the regulated release of insulin-like peptides (ILPs) during development of the C. elegans nervous system accomplishes such an integration. We find that the p38 MAP kinase PMK-3, which is required for the differentiation of chemosensory BAG neurons, functions by limiting expression of an autocrine ILP signal that represses a chemosensory-neuron fate. ILPs are released from BAGs in an activity-dependent manner during embryonic development, and regulate neurodifferentiation through a non-canonical insulin receptor signaling pathway. The differentiation of a specialized neuron-type is, therefore, coordinately regulated by a genetic program that controls ILP expression and by neural activity, which regulates ILP release. Autocrine signals of this kind may have general and conserved functions as integrators of deterministic genetic programs with activity-dependent mechanisms during neurodevelopment.

Gaseous Transmitter Regulation of Catecholamine Secretion by hypoxia in Murine Adrenal Chromaffin Cells

2021 ◽  
Author(s):  
Anna Gridina ◽  
Xiaoyu Su ◽  
Shakil A. Khan ◽  
Ying-Jie Peng ◽  
Benjamin L Wang ◽  
...  
Keyword(s):  
Nervous System ◽  
Protein Kinase ◽  
Guanylyl Cyclase ◽  
Chromaffin Cells ◽  
Soluble Guanylyl Cyclase ◽  
Protein Kinase G ◽  
Adrenal Chromaffin Cells ◽  
Wild Type ◽  
Genetic Deletion ◽  
Adrenal Chromaffin

Emerging evidence suggests that gaseous molecules, carbon monoxide (CO) and hydrogen sulfide (H2S) generated by heme oxygenase-(HO)-2 and cystathionine γ-lyase (CSE), respectively, function as transmitters in the nervous system. Present study examined the roles of CO and H2S in hypoxia-induced catecholamine (CA) release from adrenal medullary chromaffin cells (AMC). Studies were performed on AMC from adult (≥6 weeks of age) wild type (WT), HO-2 null, CSE null and HO-2/CSE double null mice of either gender. CA secretion was determined by carbon fiber amperometry and [Ca2+]i by microflurometry using Fura-2. HO-2- and CSE immunoreactivities were seen in WT AMC, which were absent in HO-2 and CSE null mice. Hypoxia (medium pO2 30-38 mmHg) evoked CA release and elevated [Ca2+]i. The magnitude of hypoxic response was greater in HO-2 null mice and in HO inhibitor treated WT AMC compared to controls. H2S levels were elevated in HO-2 null AMC. Either pharmacological inhibition or genetic deletion of CSE prevented the augmented hypoxic responses of HO-2 null AMC and H2S donor rescued AMC responses to hypoxia in HO-2/CSE double null mice. CORM-3, a CO donor, prevented the augmented hypoxic responses in WT and HO-2 null AMC. CO donor reduced H2S levels in WT AMC. The effects of CO donor were blocked by either ODQ or 8pCT, inhibitors of soluble guanylyl cyclase (SGC) or protein kinase G, respectively. These results suggest that HO-2-derived CO inhibits hypoxia-evoked CA secretion from adult murine AMC involving soluble guanylyl cyclase (SGC)-protein kinase G (PKG)-dependent regulation of CSE- derived H2S.

scholarly journals Functional Connectomics in C. elegans

2018 ◽  
Author(s):  
Elizabeth M. DiLoreto ◽  
Christopher D. Chute ◽  
Samantha Bryce ◽  
Jagan Srinivasan
Keyword(s):  
Nervous System ◽  
Information Processing ◽  
Caenorhabditis Elegans ◽  
Neural Circuits ◽  
Neuronal Function ◽  
Complete Understanding ◽  
Mutant Analysis ◽  
C Elegans ◽  
Technological Advances ◽  
Shed Light

The complete structure and connectivity of the Caenorhabditis elegans nervous system was first published in 1986. The ‘mind of a worm’ was the first organism to have its nervous system to be reconstructed at the level of synapses, and represented a critical milestone considering today it remains the only organism to be mapped to that level of connection. Recently, the extrasynaptic connectome of neuropeptides and monoamines has been described. This review discusses recent technological advances used to perturb whole-organism neuronal function, such as: whole brain imaging, optogenetics, sonogenetics and mutant analysis, which have allowed for interrogations of both local and global neural circuits, leading to different behaviors. A better understanding of a whole organism requires combining experimental datasets with biophysical neuronal modelling, and behavioral quantification. Combining these approaches will provide a complete understanding of the worm nervous system and shed light into how networks function and interact with the synaptic network to modulate information processing and behavioral output.

PKG and NHR-49 signalling co-ordinately regulate short-term fasting-induced lysosomal lipid accumulation in C. elegans

2014 ◽  
Vol 461 (3) ◽  
pp. 509-520 ◽  
Author(s):  
Wen-ming Huang ◽  
Zhao-yu Li ◽  
Yan-jun Xu ◽  
Wei Wang ◽  
Mao-ge Zhou ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Lipid Accumulation ◽  
Hormone Receptor ◽  
Nuclear Hormone Receptor ◽  
Protein Kinase G ◽  
Short Term ◽  
C Elegans ◽  
Lipids Accumulation

Short-term fasting induces lipids accumulation in the lysosome of C. elegans and the response is co-ordinately regulated by protein kinase G and nuclear hormone receptor NHR-49-mediated pathways.

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