scholarly journals Co-option of neurotransmitter signaling for inter-organismal communication in C. elegans

2018 ◽  
Author(s):  
Christopher D. Chute ◽  
Elizabeth M. DiLoreto ◽  
Ying K. Zhang ◽  
Diego Rayes ◽  
Veronica L. Coyle ◽  
...  
Keyword(s):  
Calcium Imaging ◽  
Communication Channel ◽  
Ectopic Expression ◽  
Genetic Rescue ◽  
C Elegans ◽  
Chemical Structures ◽  
Evolutionarily Conserved ◽  
Amine Neurotransmitters ◽  
Necessary And Sufficient ◽  
G Protein Coupled

AbstractBiogenic amine neurotransmitters play a central role in metazoan biology, and both their chemical structures and cognate receptors are evolutionarily conserved. Their primary roles are in intra-organismal signaling, whereas biogenic amines are not normally recruited for communication between separate individuals. Here, we show that in C. elegans, a neurotransmitter-sensing G protein-coupled receptor, TYRA-2, is required for avoidance responses to osas#9, an ascaroside pheromone that incorporates the neurotransmitter octopamine. Neuronal ablation, cell-specific genetic rescue, and calcium imaging show that tyra-2 expression in the nociceptive neuron ASH is necessary and sufficient to induce osas#9 avoidance. Ectopic expression in the AWA neuron, which is generally associated with attractive responses, reverses the response to osas#9, resulting in attraction instead of avoidance behavior, confirming that TYRA-2 partakes in sensing osas#9. The TYRA-2/osas#9 signaling system thus represents an inter-organismal communication channel that evolved via co-option of a neurotransmitter and its cognate receptor.

hlh-12, a gene that is necessary and sufficient to promote migration of gonadal regulatory cells in C. elegans, evolved within the Caenorhabditis clade

Genetics ◽  
2021 ◽  
Author(s):  
Hana E Littleford ◽  
Karin Kiontke ◽  
David H A Fitch ◽  
Iva Greenwald
Keyword(s):  
Ectopic Expression ◽  
Morphological Diversity ◽  
Nematode Species ◽  
Bhlh Protein ◽  
Vulval Development ◽  
C Elegans ◽  
Form And Function ◽  
Somatic Gonad ◽  
And Function ◽  
Necessary And Sufficient

Abstract Specialized cells of the somatic gonad primordium of nematodes play important roles in the final form and function of the mature gonad. C. elegans hermaphrodites are somatic females that have a two-armed, U-shaped gonad that connects to the vulva at the midbody. The outgrowth of each gonad arm from the somatic gonad primordium is led by two female Distal Tip Cells (fDTC), while the Anchor Cell (AC) remains stationary and central to coordinate uterine and vulval development. The bHLH protein HLH-2 and its dimerization partners LIN-32 and HLH-12 had previously been shown to be required for fDTC specification. Here, we show that ectopic expression of both HLH-12 and LIN-32 in cells with AC potential transiently transforms them into fDTC-like cells. Furthermore, hlh-12 was known to be required for the fDTCs to sustain gonad arm outgrowth. Here, we show that ectopic expression of HLH-12 in the normally stationary AC causes displacement from its normal position, and that displacement likely results from activation of the leader program of fDTCs because it requires genes necessary for gonad arm outgrowth. Thus, HLH-12 is both necessary and sufficient to promote gonadal regulatory cell migration. As differences in female gonadal morphology of different nematode species reflect differences in the fate or migratory properties of the fDTCs or of the AC, we hypothesized that evolutionary changes in the expression of hlh-12 may underlie evolution of such morphological diversity. However, we were unable to identify an hlh-12 ortholog outside of Caenorhabditis. Instead, by performing a comprehensive phylogenetic analysis of all Class II bHLH proteins in multiple nematode species, we found that HLH-12 evolved within the Caenorhabditis clade, possibly by duplicative transposition of hlh-10. Our analysis suggests that control of gene regulatory hierarchies for gonadogenesis can be remarkably plastic during evolution without adverse phenotypic consequence.

scholarly journals Phosphorylation of the microtubule-severing AAA+ enzyme Katanin regulates C. elegans embryo development

2020 ◽  
Vol 219 (6) ◽  
Author(s):  
Nicolas Joly ◽  
Eva Beaumale ◽  
Lucie Van Hove ◽  
Lisa Martino ◽  
Lionel Pintard
Keyword(s):  
Mitotic Spindle ◽  
The Other ◽  
Meiotic Spindle ◽  
Aaa Atpase ◽  
C Elegans ◽  
Microtubule Severing ◽  
Evolutionarily Conserved ◽  
Necessary And Sufficient ◽  
Fine Tune

The evolutionarily conserved microtubule (MT)-severing AAA-ATPase enzyme Katanin is emerging as a critical regulator of MT dynamics. In Caenorhabditis elegans, Katanin MT-severing activity is essential for meiotic spindle assembly but is toxic for the mitotic spindle. Here we analyzed Katanin dynamics in C. elegans and deciphered the role of Katanin phosphorylation in the regulation of its activity and stability. Katanin is abundant in oocytes, and its levels drop after meiosis, but unexpectedly, a significant fraction is present throughout embryogenesis, where it is dynamically recruited to the centrosomes and chromosomes during mitosis. We show that the minibrain kinase MBK-2, which is activated during meiosis, phosphorylates Katanin at multiple serines. We demonstrate unequivocally that Katanin phosphorylation at a single residue is necessary and sufficient to target Katanin for proteasomal degradation after meiosis, whereas phosphorylation at the other sites only inhibits Katanin ATPase activity stimulated by MTs. Our findings suggest that cycles of phosphorylation and dephosphorylation fine-tune Katanin level and activity to deliver the appropriate MT-severing activity during development.

scholarly journals EXC-4/CLIC, Gα, and Rho/Rac signaling regulate tubulogenesis in C. elegans

2021 ◽  
Author(s):  
Anthony F Arena ◽  
Daniel D Shaye
Keyword(s):  
G Protein ◽  
Small Gtpases ◽  
Loss Of Function ◽  
C Elegans ◽  
C Terminus ◽  
Evolutionarily Conserved ◽  
Rho Family Gtpases ◽  
Rho Family ◽  
Vessel Development ◽  
G Protein Coupled

The Rho-family of small GTPases, which play crucial roles in development and disease, are regulated by many signal-transduction cascades, including G-protein-coupled receptor (GPCR)-heterotrimeric G-protein (Gα/β/γ) pathways. Using genetic approaches in C. elegans we identified a new role for Gα and Rho/Rac signaling in cell outgrowth during tubulogenesis and show that the Chloride Intracellular Channel (CLIC) protein EXC-4 is an evolutionarily-conserved player in this pathway. The gene exc-4 was identified by its role in tubulogenesis of the excretory canal (ExCa) cell: a unicellular tube required for osmoregulation and fluid clearance. We identified a new exc-4 loss-of-function allele that affects an evolutionarily conserved residue in the C-terminus. Using this mutant we identified genetic interactions between exc-4, Gα's and Rho-family GTPases, defining novel roles for Gα-encoding genes (gpa-12/Gα12/13, gpa-7/Gαi, egl-30/Gαq, and gsa-1/Gαs) and the Rho-family members ced-10/Rac and mig-2/RhoG in ExCa outgrowth. EXC-4 and human CLICs have conserved functions in tubulogenesis, and CLICs and Gα-Rho/Rac signaling regulate tubulogenesis during blood vessel development. Therefore, our work defines a primordial role for EXC-4/CLICs in Gα-Rho/Rac-signaling during tubulogenesis.

scholarly journals FSHR-1/GPCR activates the mitochondrial unfolded protein response in Caenorhabditis elegans

2019 ◽  
Author(s):  
Sungjin Kim ◽  
Derek Sieburth
Keyword(s):  
Unfolded Protein Response ◽  
Mitochondrial Stress ◽  
C Elegans ◽  
Unfolded Protein ◽  
Mitochondrial Homeostasis ◽  
Evolutionarily Conserved ◽  
Genetic Deficiency ◽  
Protein Response ◽  
G Protein Coupled ◽  
Mitochondrial Unfolded Protein Response

AbstractThe mitochondrial unfolded protein response (UPRmt) is an evolutionarily conserved adaptive response that functions to maintain mitochondrial homeostasis following mitochondrial damage. In C. elegans, the nervous system plays a central role in responding to mitochondrial stress by releasing endocrine signals that act upon distal tissues to activate the UPRmt. The mechanisms by which mitochondrial stress is sensed by neurons and transmitted to distal tissues is not fully understood. Here, we identify a role for the conserved follicle-stimulating hormone G protein coupled receptor (GPCR), FSHR-1, in promoting UPRmt activation. Genetic deficiency of fshr-1 severely attenuates UPRmt activation and organism-wide survival in response to mitochondrial stress. FSHR-1 functions in a common genetic pathway with SPHK-1/sphingosine kinase to promote UPRmt activation, and FSHR-1 regulates the mitochondrial association of SPHK-1 in the intestine. Through tissue-specific rescue assays, we show that FSHR-1 functions in neurons to activate the UPRmt, to promote mitochondrial association of SPHK-1 in the intestine, and to promote organism-wide survival in response to mitochondrial stress. We propose that FSHR-1 functions cell non-autonomously in neurons to activate UPRmt upstream of SPHK-1 signaling in the intestine.

scholarly journals Mating-induced Male Death and Pheromone Toxin-regulated Androstasis

2015 ◽  
Author(s):  
Cheng Shi ◽  
Alexi M. Runnels ◽  
Coleen T. Murphy
Keyword(s):  
Ectopic Expression ◽  
Cost Of Reproduction ◽  
Male Pheromone ◽  
Male Population ◽  
Reproduction Mode ◽  
C Elegans ◽  
Evolutionarily Conserved ◽  
Chemical Messenger ◽  
Species Specific ◽  
Single Worm

AbstractHow mating affects male lifespan is poorly understood. Using single worm lifespan assays, we discovered that males live significantly shorter after mating in both androdioecious (male and hermaphroditic) and gonochoristic (male and female) Caenorhabditis. Germline-dependent shrinking, glycogen loss, and ectopic expression of vitellogenins contribute to male post-mating lifespan reduction, which is conserved between the sexes. In addition to mating-induced lifespan decrease, worms are subject to killing by male pheromone-dependent toxicity. C. elegans males are the most sensitive, whereas C. remanei are immune, suggesting that males in androdioecious and gonochoristic species utilize male pheromone differently as a toxin or a chemical messenger. Our study reveals two mechanisms involved in male lifespan regulation: germline-dependent shrinking and death is the result of an unavoidable cost of reproduction and is evolutionarily conserved, whereas male pheromone-mediated killing provides a novel mechanism to cull the male population and ensure a return to the self-reproduction mode in androdioecious species. Our work highlights the importance of understanding the shared vs. sex- and species-specific mechanisms that regulate lifespan.

scholarly journals A conserved behavioral role for a nematode interneuron neuropeptide receptor

Genetics ◽  
2021 ◽  
Author(s):  
Cynthia M Chai ◽  
Wen Chen ◽  
Wan-Rong Wong ◽  
Heenam Park ◽  
Sarah M Cohen ◽  
...  
Keyword(s):  
Interspecific Variation ◽  
Receptor Expression ◽  
Model Organisms ◽  
Closely Related Species ◽  
Behavioral Complexity ◽  
C Elegans ◽  
Evolutionarily Conserved ◽  
Cellular Context ◽  
Functional Analyses ◽  
G Protein Coupled

Abstract Neuropeptides are evolutionarily-conserved modulators of many aspects of animal behavior and physiology, and expand the repertoire of processes that can be controlled by a limited number of neurons. Deciphering the neuropeptidergic codes that govern distinct processes requires systematic functional analyses of neuropeptides and their cognate receptors. Even in well-studied model organisms like Caenorhabditis elegans, however, such efforts have been precluded by a lack of mutant reagents. Here, we generated and screened 21 C. elegans neuropeptide G-protein coupled receptor mutants with no pre-existing reagents for the touch-evoked escape response, and implicated six receptors expressed in diverse neuron classes representing multiple circuit levels in this behavior. We further characterized the mutant with the most severe phenotype, frpr-14, which was defective in multiple behavioral paradigms. We leveraged this range of phenotypes to reveal that FRPR-14 modulation of different pre-command interneuron classes, AVH and AIB, can drive distinct behavioral subsets, demonstrating cellular context-dependent roles for FRPR-14 signaling. We then show that Caenorhabditis briggsae CBR-FRPR-14 modulates an AVH-like interneuron pair to regulate the same behaviors as C. elegans but to a smaller extent. Our results also suggest that differences in touch-evoked escape circuit architecture between closely-related species results from changes in neuropeptide receptor expression pattern, as opposed to ligand-receptor pairing. This study provides insights into the principles utilized by a compact, multiplexed nervous system to generate intraspecific behavioral complexity and interspecific variation.

scholarly journals The crest phenotype in domestic chicken is caused by a 197 bp duplication in the intron of HOXC10

2021 ◽  
Author(s):  
Jingyi Li ◽  
Mi-Ok Lee ◽  
Brian W Davis ◽  
Ping Wu ◽  
Shu-Man Hsieh-Li ◽  
...  
Keyword(s):  
Gene Expression ◽  
Whole Genome Sequencing ◽  
Diagnostic Test ◽  
Genome Sequencing ◽  
Ectopic Expression ◽  
Body Region ◽  
Whole Genome ◽  
Dorsal Skin ◽  
Conserved Sequence ◽  
Evolutionarily Conserved

Abstract The Crest mutation in chicken shows incomplete dominance and causes a spectacular phenotype in which the small feathers normally present on the head are replaced by much larger feathers normally present only in dorsal skin. Using whole genome sequencing, we show that the crest phenotype is caused by a 197 bp duplication of an evolutionarily conserved sequence located in the intron of HOXC10 on chromosome 33. A diagnostic test showed that the duplication was present in all 54 crested chickens representing eight breeds and absent from all 433 non-crested chickens representing 214 populations. The mutation causes ectopic expression of at least five closely linked HOXC genes, including HOXC10, in cranial skin of crested chickens. The result is consistent with the interpretation that the crest feathers are caused by an altered body region identity. The upregulated HOXC gene expression is expanded to skull tissue of Polish chickens showing a large crest often associated with cerebral hernia, but not in Silkie chickens characterized by a small crest, both homozygous for the duplication. Thus, the 197 bp duplication is required for the development of a large crest and susceptibility to cerebral hernia because only crested chicken show this malformation. However, this mutation is not sufficient to cause herniation because this malformation is not present in breeds with a small crest, like Silkie chickens.

scholarly journals C. elegans discriminates colors to guide foraging

Science ◽  
2021 ◽  
Vol 371 (6533) ◽  
pp. 1059-1063 ◽  
Author(s):  
D. Dipon Ghosh ◽  
Dongyeop Lee ◽  
Xin Jin ◽  
H. Robert Horvitz ◽  
Michael N. Nitabach
Keyword(s):  
Stress Response ◽  
Cellular Stress ◽  
Color Discrimination ◽  
Cellular Stress Response ◽  
Blue Pigment ◽  
Natural Environments ◽  
C Elegans ◽  
Evolutionarily Conserved ◽  
Foraging Decisions ◽  
Light Guides

Color detection is used by animals of diverse phyla to navigate colorful natural environments and is thought to require evolutionarily conserved opsin photoreceptor genes. We report that Caenorhabditis elegans roundworms can discriminate between colors despite the fact that they lack eyes and opsins. Specifically, we found that white light guides C. elegans foraging decisions away from a blue-pigment toxin secreted by harmful bacteria. These foraging decisions are guided by specific blue-to-amber ratios of light. The color specificity of color-dependent foraging varies notably among wild C. elegans strains, which indicates that color discrimination is ecologically important. We identified two evolutionarily conserved cellular stress response genes required for opsin-independent, color-dependent foraging by C. elegans, and we speculate that cellular stress response pathways can mediate spectral discrimination by photosensitive cells and organisms—even by those lacking opsins.

scholarly journals The Biology of Vasopressin

Biomedicines ◽  
2021 ◽  
Vol 9 (1) ◽  
pp. 89
Author(s):  
Samantha Sparapani ◽  
Cassandra Millet-Boureima ◽  
Joshua Oliver ◽  
Kathy Mu ◽  
Pegah Hadavi ◽  
...  
Keyword(s):  
Parental Behavior ◽  
Cell Types ◽  
G Protein Coupled Receptors ◽  
Receptor Expression ◽  
Evolutionarily Conserved ◽  
Terrestrial Environments ◽  
Intracellular Vesicles ◽  
G Protein Coupled ◽  
Neuropsychiatric Conditions ◽  
Vasopressin Synthesis

Vasopressins are evolutionarily conserved peptide hormones. Mammalian vasopressin functions systemically as an antidiuretic and regulator of blood and cardiac flow essential for adapting to terrestrial environments. Moreover, vasopressin acts centrally as a neurohormone involved in social and parental behavior and stress response. Vasopressin synthesis in several cell types, storage in intracellular vesicles, and release in response to physiological stimuli are highly regulated and mediated by three distinct G protein coupled receptors. Other receptors may bind or cross-bind vasopressin. Vasopressin is regulated spatially and temporally through transcriptional and post-transcriptional mechanisms, sex, tissue, and cell-specific receptor expression. Anomalies of vasopressin signaling have been observed in polycystic kidney disease, chronic heart failure, and neuropsychiatric conditions. Growing knowledge of the central biological roles of vasopressin has enabled pharmacological advances to treat these conditions by targeting defective systemic or central pathways utilizing specific agonists and antagonists.

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