[
International C. elegans Meeting,
1991]
Some 7-alkoxy-2,2-dimethylchromenes (precocenes) adversely affect caenorhabditids. Some symptomps caused by them could partially be compensated by exogenous insect juvenile hormone analogue (JHA) methopren (Fodor et al., 1982, 1989; Fodor & Timar, 1989, Gen. Comp. Endocrinol.). Precocenes are suspected pro-mutagenes, which might be activated by epoxydases in some tissues and the JHA may act as a competitor. Whether precocenes could be used as selective agents for getting mutants resistant to free radicals, eleven biologically active analog were tested according to Szabad et al. (Mut. Res., 1981) by determining the frequency of mitotic recombination in untreated and P-- treated Drosophila melanoqaster. The results were practically negative but inconclusive, as the precocenes inactivated in the medium within a few hours. Just below its toxic concentration (at a dose of 150 ug/ml NGM medium), however, precocene II did significantly decrease the average life span of the amphimictic strain of C. remanei at 25 C from 8 days to 6. Whether the adverse effect on the life span can or cannot be compensated is under study.
[
International Worm Meeting,
2021]
Cellular stressors including heat shock and ultraviolet radiation (UV) cause sleep in the nematode Caenorhabditis elegans. This stress-induced sleep is characterized by locomotor quiescence, cessation from feeding, an increased arousal threshold, and rapid reversibility. We have identified a novel stressor which causes sleep in C. elegans: the Orsay virus. The Orsay virus is the only known virus to infect C. elegans and is related to the nodavirus, which infects other invertebrates as well as vertebrates including mammals. The Orsay virus exclusively infects intestinal cells. Despite infection of non-neuronal cells, Orsay caused sleep through a similar neuronal mechanism as sleep caused by other stressors. We hypothesized the same genetic and neural circuitry which controls sleep in response to UV and sleep would also control sleep in response to Orsay. Similar to UV and heat, mutations which affected development of the ALA neuron and processing of neuropeptides reduced sleep in infected animals. Conversely, mutations which affected development of the RIS neuron (which is required for UV/heat sleep) did not affect sleep in response to Orsay. ALA-defective animals, which had reduced sleep, had decreased survival compared to wild-type animals. This effect on survival was not observed in the RIS-defective animals, which slept normally. Transgenic overexpression of somnogenic FLP-13 neuropeptides increased the survival of infected ALA-defective animals. The survival benefit of sleeping animals was not explained by a difference in viral replication levels or in the transcriptional intracellular pathogen response. Infection with Orsay caused a decrease in global ATP levels, and this decrease was more severe in ALA-defective animals. The decreased survival of virally-infected animals was accompanied by the proliferation of OP50 bacteria inside the gut of the animal, and in some cases beyond the intestines. Lifespan was extended in virus-infected animals when they were grown on UV-killed OP50 bacteria, suggesting that bacterial superinfection is partially responsible for virus-induced lethality. These findings suggest that sleep is beneficial for recovery from infection due to its effect on energetics, and this model presents a novel opportunity to explore the protective role of sleep in host-pathogen interactions.
[
International C. elegans Meeting,
1999]
Entomopathogenic nematode (EPN)species belonging to the Steinernema and Heterorhabditis genera are closely related to C. elegans (Blaxter et al., 1998). They form an intimate symbiotic complex with bacteria Xenorhabdus spp. and Photorhabdus spp., respectively, which are closely related to E. coli . The symbiosis is developmentally regulated: there is a direct cell-cell contact between the gut cell of the (infective) dauerlarva and the primary phase variant of the symbiotic bacteria. The symbiosis is taxon specific. Individual Xenorhabdus species used as symbionts by each Steinernema species and individual strains of Photorhabdus luminescens used as symbionts by each Heterorhabditis strains belonging to different species. The phylogenetic relations between species and strains have been analysed by RFLP of the internally transcribed spacer region of the respective rRNA operon. The PCR-amplified DNAs were digested by different restriction enzymes and the restriction patterns obtained by PhastSystem PAGE were compared. On the basis of the comparative analysis of the ITS1 - ITS2 patterns nematodes could be identified at species level. Xenorhabdus species could also be identified on the basis of the comparative analysis of the spacer region of the 16S - 23S rRNA operon. P. luminescens strains, belonging to different subclusters (Szallas et al., 1997) could be separated on the basis of the RFLP pattern of the spacer region of the 16S - 23S rRNA operon. Adams, B.J. (1998). Species conception and the evolutionary paradigm in modern nematology. J. nematol. 30, 1-21. Adams, B.J., Burnell, A.M. @ Powers,T.O. (1998). A phylogenetic analysis of Heterorhabditis based on ITS 1 DNA sequence data. J. nematol. 30, 22-39. Blaxter,R. et al.(1998).Molecular evolutionary framework for Phylum nematoda. Nature 392,71-75. Szallas E., Koch, H., Fodor,A.,Szentirmai, A., Nealson,K.H. Stackebrandt, E.(1997).Phylogenetic evidence for taxonomic heterogeneity of P.luminescens. IJSB 47, 402-407.