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Tina Burton et al. (2007) International Worm Meeting "Role of the flp neuropeptide gene family in C. elegans."

Zi Huang, Tina Burton, Adewale Olajubelo, Jenny Chang, Lawrence Ha, Chris Li

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International Worm Meeting,

2007]

Neuropeptides are short sequences of amino acids that are used in the nervous system to modulate behavior. Because a single neuropeptide can have multiple functions and because multiple neuropeptides can impact the same behaviors, the precise roles of specific neuropeptides in different behaviors have been difficult to assess. We are examining the function, regulation, and signaling pathways of the flp neuropeptide gene family in C. elegans. At least 30 flp genes encode peptides from the FMRFamide (Phe-Met-Arg-Phe-amide) family. To determine the function of the different flp genes, we are isolating deletion mutants for each gene. Thus far, mutations have been identified in 11 flp genes. The mutants are being screened for defects in locomotion, reproduction, and development. We have found that each flp mutant is defective on at least one assay, and several mutants are defective in multiple assays. The number of mutants showing defects on these assays is somewhat surprising, particularly given their expression patterns. To verify that these phenotypes are due to loss of the flp gene, we are performing transgenic rescue. However, we are unable to isolate stable transgenic lines for several flp genes. Because the increased transgenic expression may be toxic to the animals, we are currently decreasing the amount of injected DNA to isolate stable transformants. These data suggest that locomotion, reproduction, and development are finely tuned by levels of the different FLP neuropeptides. In addition, we are characterizing animals carrying mutations in known FLP receptors. Insights into how neuropeptides function in C. elegans may give clues into how neuropeptides are used in higher animals and into the design of antihelminthic drugs.

Burton, Nicholas et al. (2013) International Worm Meeting "Antagonistic cGMP Signaling Pathways Regulate a Heritable Developmental Response to Pathogens."

Burton, Nicholas, Horvitz, Bob

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International Worm Meeting,

2013]

Recently a number of studies have linked environmental stress to changes in the physiology of an individual's progeny. To test whether maternal infection affects progeny, we fed C. elegans either Pseudomonas aeruginosa (PA14) or Serretia marcesens (DB10). We found that wild-type parental (P0) worms slow their rate of development when fed either PA14 or DB10 in comparison to OP50. In the following generation, when again exposed to pathogen, the progeny (F1) exhibit a dramatically enhanced slowing of development compared to that of naive worms. However, when the progeny of infected worms are fed OP50, they exhibit no difference in developmental rate compared to naive worms, indicating that both the P0 and F1 require exposure to pathogen to result in enhanced slowing. We showed that developmental slowing requires the guanylyl cyclase GCY-36 and the cGMP-dependent kinase EGL-4 as well as the insulin-like peptide INS-7. In contrast to worms unable to slow their development, worms lacking either the guanylyl cyclase GCY-33 or the serotonin biosynthetic enzyme TPH-1 exhibit an enhanced slowing of development. In the case of gcy-33, this enhancement can be suppressed by mutations in gcy-36 and egl-4. (Zimmer et, al. Neuron 61 865, 2009), showed that gcy-33 acts together with gcy-31 to mediate responses to low oxygen and that gcy-36 acts together with gcy-35 to mediate responses to high oxygen. They also showed that gcy-33, gcy-35 and gcy-36 promoters drive expression in AQR, PQR and URX neurons. The gcy-31 promoter, however, does not. Interestingly, we observed that mutations in gcy-31 do not affect development in response to PA14. Furthermore, we found that genetic ablation of AQR, PQR and URX results in a similar phenotype to that of gcy-33 mutants. These results suggest that the defect in developmental rate of gcy-33 mutants is separable from the defect in the response to low oxygen. In summary, we have found that parental bacterial infection influences the development of progeny and that antagonistic cGMP signaling pathways regulate this response at least in part through the AQR, PQR, and URX neurons.

Tina Burton et al. (2006) Neuronal Development, Synaptic Function, and Behavior Meeting "Multiple FLPs are Involved in Locomotion and Egg-laying Behaviors"

Tina Burton, Lawrence Ha, Jenny Chang, Chris Li, Diego Levy, Adewale Olajubelo

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Neuronal Development, Synaptic Function, and Behavior Meeting,

2006]

Neuropeptides are involved in all complex behaviors in mammals. FMRFamide and related peptides (FaRPs) all share a common Arg-Phe-amide at their C-termini, and are found in organisms throughout the animal kingdom, where they are involved in a variety of behaviors, including cardioactivity, pain modulation, and reproduction. At least 29 flp genes encode over 70 FaRPs in C. elegans. Each flp gene encodes a unique set of peptides and is expressed in a distinct set of cells. Most, if not all, of the predicted FLP peptides are produced, and signal through G protein coupled receptors. To determine the role of the flp genes, we have been isolating animals carrying deletions in the different flp genes, and examining the mutants for locomotory and egg-laying defects. To date, we have isolated 11 flp mutants. Surprisingly, eight of the flp mutants have defects in locomotion and seven are egg-laying defective, suggesting that many FLP peptides modulate these behaviors. Furthermore, five flp mutants are resistant to serotonin-induced sluggishness. We have also been characterizing mutants carrying deletions in G protein coupled receptors, including some of the FLP receptors. These animals also have defects in locomotion and egg laying. The potential complexity with which the FLPs modulate certain behaviors is enormous and awaits further examination.

Burton, Nick et al. (2021) International Worm Meeting "Intergenerational adaptations to stress are evolutionarily conserved, stress specific, and have deleterious trade-offs"

Fisher, Kinsey, Stevens, Lewis, Baugh, L. Ryan, Willis, Alexandra, Miska, Eric, Reinke, Aaron, Price, Jon, Braukmann, Fabian, Burton, Nick

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International Worm Meeting,

2021]

Despite reports of parental exposure to stress promoting adaptations in progeny in diverse organisms, there remains considerable debate over the ecological significance and evolutionary conservation of these multigenerational effects. Here, we investigate four independent examples of intergenerational adaptations to stress in C. elegans - bacterial infection, microsporidia infection, osmotic stress and starvation - across four different Caenorhabditis species. We found that all four intergenerational adaptations to stress are conserved in at least one other species, that the responses and evolutionary conservation patterns are stress specific, and that intergenerational adaptive effects have deleterious trade-offs in mismatched environments. By profiling the intergenerational and transgenerational effects of different stresses on gene expression across species, we identified 3,174 genes that exhibited intergenerational changes in expression in multiple species in response to stress. Furthermore we found that an inversion in the expression of certain stress response genes required for intergenerational adaptations, from increased expression in the offspring of stressed parents to decreased expression in the offspring of stressed parents, correlates with an inversion of an adaptive response to infection in C. elegans and C. kamaaina to a deleterious intergenerational effect in C. briggsae. By contrast, we did not observe any conserved transgenerational changes in gene expression in response to stress, suggesting that the intergenerational effects of stress on offspring gene expression are not maintained transgenerationally. Our results demonstrate that intergenerational responses to stress play a substantial, evolutionarily conserved, and largely reversible role in regulating animal physiology.

Barbara Meyer (2008) Development & Evolution Meeting "Gametogenesis, Meiosis, & Sex Determination"

Barbara Meyer

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