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[
Am J Hum Genet,
1998]
Since Sydney Brenner wrote this statement in a visionary research proposal addressed to Max Perutz 35 years ago, an enormous amount of information has been gathered on the biology of the nematode Caenorhabditis elegans ("the worm"), both fulfilling his predictions and exceeding his original expectations. Researchers have identified every cell in the worm and have described all the lineages by which these cells are formed...
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[
Worm Breeder's Gazette,
1992]
unc-4 LacZ expression in A-type motor neurons David M. Miller and Charles J. Niemeyer, Dept. of Cell Biology, Duke Univ. Medical Ctr, Durham, NC 27710
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[
J Bacteriol,
2014]
Volume 195, no. 16, p. 35143523, 2013. A number of problems related to images published in this paper have been brought to our attention. Figure 1D contains duplicated images in lanes S and LE, and Fig. 4D and 6B contain images previously published in articles in this journal and in Microbiology and Microbial Pathogenesis, i.e., the following: C. G. Ramos, S. A. Sousa, A. M. Grilo, J. R. Feliciano, and J. H. Leitao, J. Bacteriol. 193:15151526, 2011. doi:10.1128/JB.01374-11. S. A. Sousa, C. G. Ramos, L. M. Moreira, and J. H. Leitao, Microbiology 156:896908, 2010. doi:10.1099/mic.0.035139-0. C. G. Ramos, S. A. Sousa, A. M. Grilo, L. Eberl, and J. H. Leitao, Microb. Pathog. 48:168177, 2010. doi: 10.1016/j.micpath.2010.02.006. Therefore, we retract the paper. We deeply regret this situation and apologize for any inconvenience to the editors and readers of Journal of Bacteriology, Microbial Pathogenesis, and Microbiology.
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Kaleta, C., Li, C.C.Y., Casanueva, O, Le Novere, N., Witting, M., Hastings, J.
[
International Worm Meeting,
2017]
C. elegans has recently been advanced as a premier metazoan model organism for the study of metabolism, with the publication of two whole-genome metabolic models (1, 2). Using these models together with -omics data allows the in-depth data-driven exploration of systems-level metabolism using in silico simulations. In a GENiE workshop to be held April 2017 at the Babraham Institute, Cambridge, UK, the relationships between these two existing metabolic models will be explored with the objective of generating a consensus model. Because the two reconstructions are still incomplete, and certain important pathways and areas of metabolism are currently under-annotated, we aim to identify specific areas that are relevant to the C. elegans community and prioritise them for further annotation in a follow-up community-driven "annotation jamboree" workshop. This poster will describe the main objectives set by the first workshop and opens the invitation to the C. elegans metabolic research community to contribute to the follow-up annotation efforts. 1. Gebauer, J.; Gentsch, C.; Mansfeld, J.; Schmei beta er, K.; Waschina, S.; Brandes, S.; Klimmasch, L.; Zamboni, N.; Zarse, K.; Schuster, S.; Ristow, M.; Schauble, S. & Kaleta, C. (2016), 'A Genome-Scale Database and Reconstruction of Caenorhabditis elegans Metabolism.', Cell Syst 2(5), 312--322. 2. Yilmaz, L. S. & Walhout, A. J. M. (2016), 'A Caenorhabditis elegans Genome-Scale Metabolic Network Model.', Cell Syst 2(5), 297--311.
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[
Science,
2000]
Protein interaction mapping using large-scale two-hybrid analysis has been proposed as a way to functionally annotate large numbers of uncharacterized proteins predicted by complete genome sequences. This approach was examined in Caenorhabditis elegans, starting with 27 proteins involved in vulval development. The resulting map reveals both known and new potential interactions and provides a functional annotation for approximately 100 uncharacterized gene products. A protein interaction mapping project is now feasible for C. elegans on a genome-wide scale and should contribute to the understanding of molecular mechanisms in this organism and in human diseases.AD - Massachusetts General Hospital Cancer Center, Charlestown, MA 02129, USA.FAU - Walhout, A JAU - Walhout AJFAU - Sordella, RAU - Sordella RFAU - Lu, XAU - Lu XFAU - Hartley, J LAU - Hartley JLFAU - Temple, G FAU - Temple GFFAU - Brasch, M AAU - Brasch MAFAU - Thierry-Mieg, NAU - Thierry-Mieg NFAU - Vidal, MAU - Vidal MLA - engID - 1 R21 CA81658 A 01/CA/NCIID - 1 RO1 HG01715-01/HG/NHGRIPT - Journal ArticleCY - UNITED STATESTA - ScienceJID - 0404511RN - 0 (Genetic Vectors)RN - 0 (Helminth Proteins)RN - 0 (LIN-35 protein)RN - 0 (LIN-53 protein)RN - 0 (Repressor Proteins)RN - 0 (Retinoblastoma Protein)SB - IM
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[
International Worm Meeting,
2019]
The development of Caenorhabditis elegans is very robust and it takes two days to reach adulthood under standard laboratory conditions. However, in the wild, developing animals face many challenges that are not necessarily present in a sterile and controlled laboratory environment, such as pathogen stress and dietary limitations. We investigated how development is influenced by pathogen stress using C. elegans larvae and 35 Pseudomonas aeruginosa strains under modified slow-killing conditions. We observed that C. elegans larvae exhibit three developmental phenotypes when fed with different P. aeruginosa strains: normal development, slow development and very slow development. Normal and slow development are classified as reaching adulthood in 2 days and 3 days, respectively; the third group causes extreme developmental slowing and P. aeruginosa strain CF18 fed larvae do not reach adulthood. To determine the mechanism of very slow development caused by CF18, we investigated three possible mechanisms: larval gut colonization status, bacterial nutrient deficiencies and pathogenesis/toxins1,2. We found that the larva's gut is not colonized by CF18. The larvae were able to reach adulthood on UV radiated CF18 lawn, suggesting that it is not nutrient deficiency but the pathogenicity of the strain that causes this developmental slowing. Secreted compounds by CF18 in the medium were also required for the very slow development phenotype. To determine the bacterial effectors causing this developmental delay, we have generated a transposon insertion library in the CF18 background and examined the developmental phenotype of larvae when fed with these mutants. We have found that transposon insertion in certain bacterial genes, including quorum sensing and two-component system genes, allow C. elegans larvae to overcome developmental slowing. 1. Tan, M.-W., Mahajan-Miklos, S. & Ausubel, F. M. Killing of Caenorhabditis elegans by Pseudomonas aeruginosa used to model mammalian bacterial pathogenesis. Proc. Natl. Acad. Sci. 96, 715-720 (1999). 2. Watson, E. et al. Interspecies systems biology uncovers metabolites affecting C. elegans gene expression and life history traits. Cell 156, 759-770 (2014).
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[
International Worm Meeting,
2017]
Extracellular vesicles are emerging as an important aspect of intercellular communication by delivering a parcel of proteins, lipids even nucleic acids to specific target cells over short or long distances (Maas 2017). A subset of C. elegans ciliated neurons release EVs to the environment and elicit changes in male behaviors in a cargo-dependent manner (Wang 2014, Silva 2017). Our studies raise many questions regarding these social communicating EV devices. Why is the cilium the donor site? What mechanisms control ciliary EV biogenesis? How are bioactive functions encoded within EVs? EV detection is a challenge and obstacle because of their small size (100nm). However, we possess the first and only system to visualize and monitor GFP-tagged EVs in living animals in real time. We are using several approaches to define the properties of an EV-releasing neuron (EVN) and to decipher the biology of ciliary-released EVs. To identify mechanisms regulating biogenesis, release, and function of ciliary EVs we took an unbiased transcriptome approach by isolating EVNs from adult worms and performing RNA-seq. We identified 335 significantly upregulated genes, of which 61 were validated by GFP reporters as expressed in EVNs (Wang 2015). By characterizing components of this EVN parts list, we discovered new components and pathways controlling EV biogenesis, EV shedding and retention in the cephalic lumen, and EV environmental release. We also identified cell-specific regulators of EVN ciliogenesis and are currently exploring mechanisms regulating EV cargo sorting. Our genetically tractable model can make inroads where other systems have not, and advance frontiers of EV knowledge where little is known. Maas, S. L. N., Breakefield, X. O., & Weaver, A. M. (2017). Trends in Cell Biology. Silva, M., Morsci, N., Nguyen, K. C. Q., Rizvi, A., Rongo, C., Hall, D. H., & Barr, M. M. (2017). Current Biology. Wang, J., Kaletsky, R., Silva, M., Williams, A., Haas, L. A., Androwski, R. J., Landis JN, Patrick C, Rashid A, Santiago-Martinez D, Gravato-Nobre M, Hodgkin J, Hall DH, Murphy CT, Barr, M. M. (2015).Current Biology. Wang, J., Silva, M., Haas, L. A., Morsci, N. S., Nguyen, K. C. Q., Hall, D. H., & Barr, M. M. (2014). Current Biology.
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[
Biochemistry,
1987]
The major intestinal esterase from the nematode Caenorhabditis elegans has been purified to essential homogeneity. Starting from whole worms, the overall purification is 9000-fold with a 10% recovery of activity. The esterase is a single polypeptide chain of Mr 60,000 and is stoichiometrically inhibited by organophosphates. Substrate preferences and inhibition patterns classify the enzyme as a carboxylesterase (EC 3.1.1.1), but the physiological function is unknown. The sequence of 13 amino acid residues at the esterase N- terminus has been determined. This partial sequence shows a surprisingly high degree of similarity to the N-terminal sequence of two carboxylesterases recently isolated from Drosophila mojavensis [Pen, J., van Beeumen, J., & Beintema, J. J. (1986) Biochem. J. 238, 691-699].