5 Papers found (0.017 seconds)

Ravichandiran Kumarasamy et al. (2002) European Worm Meeting "Dna polymorphism in Pristionchus pacificus"

[

European Worm Meeting,

2002]

To understand the evolution of developmental process at the microevolutionary level, it is important to study the biogeography and the evolutionary alterations of the developmental processes in detail. To acuminate this, we are working on the satellite model Pristionchus pacificus. The genus Pristionchus has a worldwide distribution and different strains of Pristionchus pacificus exist from Washington (PS 1843), Hawaii (JU 138), Ontario (AF 8130), Poland (RS 106) and the wild type strain from California (PS 312). Previous AFLP studies showed a high degree of polymorphisms between the strains from Washington, Hawaii and California. BAC end sequencing and SSCP analysis of BAC end fragments between the strains from California and Washington confirmed these original observations. To obtain a better picture of the distribution of polymorphisms between the strains of P. pacificus, we have chosen a random 5 Kb region on Chromosome III that contains no open reading frame. Our results showed a high degree of polymorphism (3.46%) in both Washington and Hawaii when compared to the laboratory strain California. There were ~ 0.7% transitions, ~ 0.5% transversions, ~ 0.3% insertions and ~ 0.1% deletions. Most of the polymorphisms observed were single base pair events except a few which were up to 5 bp . Further studies are underway to extend this study, comparing the ceh-20 and ceh-40 genes in these strains and to eventually include the different species' of Pristionchus namely P. maupasi and P. lheritieri.

Chris Link et al. (2007) International Worm Meeting "Using C. elegans for in vivo structure/function analysis of beta amyloid peptide toxicity."

Chris Link, Christine Roberts, David Merin, Gin Fonte

[

International Worm Meeting,

2007]

Expression of human beta amyloid peptide (Abeta), causally implicated in Alzheimers disease, in C. elegans body wall muscle results in a robust paralysis phenotype that provides a convenient readout for Abeta toxicity. We have engineered C. elegans to express wild type Abeta 1-42 or single amino acid variants thereof to test models of Abeta toxicity. One such model is the formation of membrane pores via Abeta oligomerization driven by glycine zipper interactions between alpha helical regions of Abeta monomers (Kim S, Jeon TJ, Oberai A, Yang D, Schmidt JJ, Bowie JU. 2005. Proc Natl Acad Sci U S A 102: 14278-83). Transgenic worms expressing Abeta with a Gly37-to-Leu substitution, predicted to disrupt glycine zipper interactions, show a dramatic reduction in paralysis relative to worms expressing wild type Abeta. In addition to this reduction in paralysis, Abeta G37L worms did not show the muscle cell calcium perturbations or abnormal mitochondria observed in worms expressing wt Abeta. Immunoblot and immunohistochemical analysis demonstrates that the Abeta G37L strain has Abeta levels and cellular distribution indistinguishable from control wt Abeta strains, indicating that this reduced toxicity is due to a qualitative difference in the Abeta G37L peptide. Studies with transgenic worms co-expressing wt and G37L Abeta reveal that the Abeta G37L peptide can be anti-toxic, suggesting a dominant negative effect consistent with the variant peptide interfering with toxic oligomerization of wt Abeta. To test the oligomer model more directly, we engineered second site substitutions in the Abeta G37L peptide that based on the proposed structural model could potentially restore the predicted glycine zipper interface. Two of these second site mutations (N27G and M35G) restore toxicity to the G37L variant, strongly supporting the toxic oligomer model. These studies support the oligomer pore mechanism and identify the glycine zipper interface as a potential target for therapeutic drugs.

Kim JS et al. (1973) Kisaengchunghak Chapchi "Ecology of filariasis on Che Ju Island."

Lee WY, Kim JS, Chun SL

[

Kisaengchunghak Chapchi,

1973]

Study of filariasis to determine important factors involved in its ecology was carried out on Che Ju Island for three consecutive years from 1968 to 1970 in seven villages, three coastal villages and four islets remote from the main island. One village which was located in mountainous area far from the coast was surveyed to serve as control area. About 90% of population inhabiting the study area had at least one blood smear during the three-year period; about one third had three blood smears, and a little over one third had two, and the rest only one examination. Animal and mosquito surveys were carried out at the same period. Followings are the results obtained: 1. All human cases but several had microfilariae identical to the description of B. malayi. The several cases who had morphologically different microfilariae from that of B. malayi need further study for definite conclusion. 2. Five persons randomly sampled from Mf positives and bled every two hours demonstrated nocturnal periodicity between 9 p.m. and 3 a.m. 3. Human is considered to be only reservoir host for human filariasis in the area since animal survey and experimental exposure to the infective larvae of human filaria species showed failure to infect animals. 4. Microfilaria rate, microfilaria density, prevalence of elephantiasis varied by area and age with correlation, which indicated cumulative process of the parasite by repeated exposure and development of host immunity to certain extent. 5. Clinical manifestation of filariasis (symptom complex and elephantiasis ) taken from history and inspection was low in its prevalence with range of 0.9% 11.8% of total population. Only 5.2% of 517 Mf positives had the clinical manifestation. 24.8% of 109 persons with clinical manifestation had microfilaria; 42.9% with symptom complex only, 23.1% with both symptoms and elephantiasis, and none with elephantiasis only were microfilaria positive. 6. Ae. togoi was the only species infected with the filaria. Mosquito infection rate by area showed positive correlation to the Mf rate and density of human population; where the Mf rate and density were high, the mosquito infection rate also high.

Jung, Yoonji et al. (2021) International Worm Meeting "A Golgi protein MON-2/MON2 mediates longevity via upregulating autophagy"

[

International Worm Meeting,

2021]

The Golgi apparatus is a crucial organelle for post-translational modification and transport of macromolecules, including proteins and lipids. Impaired functions of the Golgi complex cause various diseases but its role in organismal longevity remains elusive. Here, we show that an evolutionarily conserved Golgi protein MON-2, a mediator of trafficking between endosome and the Golgi, promotes longevity caused by inhibition of mitochondrial respiration. By performing quantitative proteomics followed by RNAi-based lifespan screen, we identified factors that are required for the extended lifespan of the respiration isp-1(qm150) and clk-1(qm30) mutants. Among them, we found that genetic inhibition of mon-2 by RNAi and mutation suppressed the longevity of the respiration mutants. We showed that other factors that mediate trafficking between the Golgi and the endosome, such as snx-3/sorting nexin 3, tbc-3/TBC1D22A and PAD-1/DOP1, were also required for the longevity of respiration mutants. Next, we asked how two organelles, the Golgi and mitochondria, communicated with each other for the regulation of longevity. We hypothesized that MON-2 and established pro-longevity factors coordinately mediate the longevity of mitochondrial mutants. We demonstrated that MON-2 was required for enhancing autophagy, a process essential for long lifespan of respiratory mutants. We found that the number of LGG-1 puncta, a reporter of autophagy, was increased by isp-1(qm150) and clk-1(qm30) but decreased by mon-2(xh22) mutation. We further showed that MON-2 was required for the long lifespan caused by several regimens that upregulate autophagy, such as mutations in insulin/IGF-1 receptor, daf-2(e1370), dietary restriction mimetic eat-2(ad1116) and food deprivation. We found that HLH-30/TFEB and BEC-1/Atg6, key regulators of autophagy, promoted longevity by acting together with MON-2. We then showed that mammalian MON2 also upregulated autophagy under starvation conditions by binding to GABARAP L2, a member of LC3 family proteins. Interestingly, we found that starvation induced the translocation of MON2 from the Golgi to recycling endosome, which may contribute to autophagosome formation in cultured mammalian cells. Thus, evolutionarily conserved MON-2/MON2 appears to promote longevity via upregulating autophagy. Altogether our study highlights the crucial roles of inter-organelle communications between mitochondria, the Golgi and autophagosome in the regulation of longevity.

Ravi Kumarasamy et al. (2003) International Worm Meeting "Single Nucleotide Polymorphisms in the genus Pristionchus"

Ralf Sommer, Ravi Kumarasamy

[

International Worm Meeting,

2003]

Elaborate studies on the biogeography and the evolutionary alterations of developmental processes are of paramount importance, to understand the evolution of developmental processes at the microevolutionary level. To acuminate this, we use Pristionchus pacificus as a model system. The genus Pristionchus has a worldwide distribution and different strains of Pristionchus pacificus exist from Washington (PS 1843), Hawaii (JU 138), Ontario (AF 8130), Poland (RS 106) and the wild type strain from California (PS 312). Previous AFLP studies revealed a high degree of polymorphisms between the strains of Washington, Hawaii and California (Srinivasan etal., 2001). BAC end sequencing and SSCP analysis of BAC end fragments between the strains of California and Washington confirmed these original observations. To obtain a better picture of the distribution of polymorphisms between the strains of P. pacificus, we chose a random 5 Kb region on Chromosome III that contains no open reading frames. We observed a high degree of polymorphism (3.46%) in both Washington and Hawaii when compared to the laboratory strain California. To extend this study to regions containing a gene, we worked on two genes, namely ceh-20 and ceh-40. In C. elegans ceh-20 and ceh-40, orthologues of Drosophila Extradenticle are on Chromosomes III and I, respectively. Interestingly, in P. pacificus both these genes are on Chromosome III and on the same BAC . PCR analysis indicated that ceh-40 is 600 bp upstream of ceh-20. Both the genes are SL1 spliced and do not seem to be within one operon. Sequencing the two genes from the laboratory strains of P. pacificus indicated an approximate ~3% polymorphism, predominantly in the non-coding regions, a diversity pattern similar to the recent findings in Drosophila melanogaster and Human. In contrast, the most divergent strains of C. elegans, Bristol (N2) and Hawaii (CB 4856) show 1 SNP in 873 bp (Wicks etal., 2001). To obtain a better understanding of the polymorphism level in other species of Pristionchus, namely P. maupasi and P. lheritieri, we cloned these two genes by degenerate PCR. Comparison of sequences of the 2 genes in the different closely related species would give a better insight into the degree of polymorphisms in this genus. 1. Srinivasan, J., Pires-da silva, A., Gutierrez, A., Zheng, M., Jungblut, B., Witte, H., Schlak, I and Sommer, R.J (2001) Evol. Dev 3(4), 229-240. 2. Wicks, S.R., Yeh, R.T., Gish, W.R., Waterston, R.H and Plasterk, R.H.A (2001) Nature genetics., 28 : 160-164.