Mark Edgley et al. (2007) International Worm Meeting "At least a yeast genome's worth of KO's: report on the number of genes with mutations in C. elegans."

Don Moerman, Jeff Holmes, Gary Moulder, Mark Edgley, John Rummage, Others To Be Named, Bob Barstead, Stephane Flibotte, Jason Maydan

[International Worm Meeting, 2007]

The C. elegans Gene Knockout Consortium (http://www.celeganskoconsortium.omrf.org/) pursues systematic targeted gene disruption in the nematode, both upon request from the research community and in the larger context of the whole set of genes for which human orthologs exist (more than 7,000 genes). We are also now working on nematode specific genes. Previously our work was solely based on a reverse-genetics PCR method to generate single-gene deletions. More recently we have incorporated array Comparative Genome Hybridization (array-CGH) for efficient generation of deletion mutations (see abstract by Maydan et al). The combined strategies of directed and non-directed approaches are improving our throughput and broadening the types of mutations we can identify. All deletions isolated by the consortium are stabilized as homozygous or balanced heterozygous strains, deletion breakpoints are sequenced, and the strains and data are placed immediately into the public domain through our collaborators at the Caenorhabditis Genetics Center and WormBase. Distribution of Consortium strains accounts for a significant proportion of distributions from the CGC and has stood at 20% for the past two calendar years. To date the Consortium has generated deletions in more than 2,300 genes, and most of these have been stabilized and archived at the CGC. In addition, using CGH methodology we have identified over 700 genes missing in either the Hawaiian or Madeiran strains and consequently these genes will not be targeted for deletion by the consortium. Obtaining deletions in all genes in this nematode is the goal of the consortium and the general worm community. The combined efforts of the consortium, the Mitani lab and individuals within the worm community are moving us closer to this goal - analysis of 7205 mutations yields a very conservative estimate of about 5,000 genes with associated deletions. To put this in perspective the nematode community has now matched the yeast community whole genome effort of 5,500 KO''s.

Martinelli SD et al. (1995) International C. elegans Meeting "ACEDB"

Durbin RM, Martinelli SD

[International C. elegans Meeting, 1995]

We hope to provide a demonstration of the current state of the ACeDB worm database on Unix workstations, and if possible Apple Macintosh, throughout the poster sessions. This will be based on the new version 4 release of the acedb software (Jean Thierry-Mieg, Richard Durbin and numerous others), which contains many new features for greater efficiency, more flexible printing, and display of new features.

Masamitsu Fukuyama et al. (2002) West Coast Worm Meeting "Germline precursor cells arrest at G2/prophase during embryogenesis and dauer diapause"

Joel H Rothman, Masamitsu Fukuyama

[West Coast Worm Meeting, 2002]

We and others previously reported that the cki-1 gene, which encodes a CIP/KIP cyclin-dependent kinase inhibitor (CKI), is required for many somatic cells to exit from the embryonic cell cycle at the proper time. In contrast, we found that the two germline precursors (Z2/Z3 cells) undergo cell cycle arrest by a cki-1-independent mechanism during embryogenesis. Since CIP/KIP CKIs have been shown to be essential for developmental G1 arrest in many animals, we tested the hypothesis that the Z2/Z3 cells become mitotically quiescent at a non-G1 phase.

Seung-Jae Lee et al. (2008) C.elegans Aging, Stress, Pathogenesis, and Heterochrony Meeting "The Deadly Sweet Tooth"

Seung-Jae Lee, Cynthia Kenyon

[C.elegans Aging, Stress, Pathogenesis, and Heterochrony Meeting, 2008]

We and others have found that worms fed 2% glucose have a shortened lifespan. In this talk, I will discuss what we know about the underlying mechanism, and why we think that glycerol might play an important role in the response to glucose, and also in the coordination of the aging rates of different tissues in the animal.

M Sarkissian et al. (1999) International C. elegans Meeting "A mut-6 screen for RNAi deficient mutants"

M Sarkissian, CC Mello, H Tabara

[International C. elegans Meeting, 1999]

To investigate the mechanism of RNAi, we have undertaken genetic screens for R NA i d eficient mutants (tentatively named rid -loci). EMS mutagenesis has already yielded at least several RNAi resistant mutant strains (see the abstract by Tabara et al.). rid -mutants arise at knock out frequency and most appear to be recessive in nature. We therefore decided to search for transposon induced alleles that might be useful in cloning the rid - mutant genes. 100,000 mut-6 , lin-2 worms were allowed to grow on E.Coli expressing dsRNA for a maternal gene ( pos-1 ). One round of enrichment was carried out and the worms were replaced on the bacteria expressing the dsRNA. Thus far 14 viable strains have been obtained and a secondary microinjection based screen is now underway. So far one mut-6 strain appears to exhibit complete resistance to both maternal and zygotic RNAi. We hope to report on further genetic mapping and clonng of these mutants.

Terashima K et al. (1997) International C. elegans Meeting "EXPRESSION PATTERNS OF RNA BINDING PROTEINS IN C. ELEGANS"

Terashima K, Sakamoto H, Ohta A, Tanaka YU

[International C. elegans Meeting, 1997]

We are interested in the biological functions of RRM (RNA recognition motif)-containing RNA binding proteins and chose C. elegans as a model organism to elucidate their temporal and spatial expression patterns. For this purpose, we exploited the huge amount of sequence information of its genome currently available with which many putative RRM proteins can readily be predicted. We made GFP- and LacZ-fusion constructs of five different RRM protein genes under the control of their putative native promoters, microinjected them into C. elegans and analyzed their expression. Of the five RRM proteins analyzed, two (F35H8.5 and R10E9.1) appeared to be expressed in specific neurons as expected from their similarity to the vertebrate neuron-specific proteins HuD and Nrp1. C33H5.12 protein, which is similar to a mammalian splicing factor SRP20, was found to be expressed in muscle cells, suggesting that it might be involved in the muscle-specific splicing. Surprisingly, the cSAP49 protein, which was named because of its similarity to the mammalian spliceosome-associated protein 49, was mainly expressed in intestinal cells, although its mammalian counterpart is thought to be an essential splicing factor, and therefore is expected to be expressed in all cells. The 1243 protein, which shows no noticeable homology with known proteins, was expressed mainly in hypodermal and intestinal cells. Detailed characterization of cells expressing these genes is in progress.

Avery L et al. (1995) International C. elegans Meeting "C ELEGANS INTERNET SERVERS"

Steward K, Avery L

[International C. elegans Meeting, 1995]

Information about C elegans and the community of C elegans researchers can be found on the international computer network called the Internet. The Internet complements other information sources such as the Worm Community System (WCS) and acedb by providing a channel for diverse, rapidly changing information and for individual expression. Most universities offer free or low-cost Internet connections; commercial accounts are available to others. The software is free and runs on inexpensive models of all common classes of computers (MacIntosh, IBM-compatible, and unix).

A. Shorto et al. (2006) European Worm Meeting "Dauer Larvae Development and Fitness: Does it All Depend on your Environment?"

A. Shorto, S. C. Harvey, M. E. Viney.

[European Worm Meeting, 2006]

?. A. Shorto, S. C. Harvey and M. E. Viney. Natural isolates (including N2 and DR1350) of the free-living nematode Caenorhabditis elegans vary in their phenotypic plasticity of dauer larvae development. For example, some lines appear to be highly sensitive to dauer inducing conditions while others are less so. We have sought to investigate the causes and consequences of this plasticity.. To determine the fitness consequences of this plasticity of dauer development we have investigated how lifespan, total fecundity, reproductive schedule and population growth vary in N2 and DR1350 and in N2 x DR1350 recombinant inbred lines (RILs). We have found that the plasticity of dauer larvae development is positively correlated with the population growth rate (as measured by population size after 8 days of growth). Differences in population growth appear not to be dependent on lifetime fecundity or reproductive schedule (number of eggs laid per day) per se, but rather due to how the reproductive schedule changes in response to reduced food availability. Overall, these results suggest that there may be different reproduction and dauer formation strategies in response to environmental change.

Jacopo Novelli et al. (2002) European Worm Meeting "Genetic and molecular characterisation of two new dumpy genes: dpy-31 and dpy-32"

Jacopo Novelli, Jonathan Hodgkin, Nathalie Pujol

[European Worm Meeting, 2002]

In C. elegans there are many genes that have mutant non-lethal phenotypes affecting body size and shape. Mutations in dpy (dumpy) genes cause a short and fat body phenotype. To date, more than 30 dpy genes have been defined. Many dpy genes have been already cloned and have been shown to be involved in cuticle formation or function. Some genetically identified loci encode collagen genes, such as dpy-2, dpy-7, dpy-10 and dpy-13. Others, such as dpy-18 and dpy-11, encode enzymes responsible for posttranslational modification or assembly of collagen molecules. At least one dpy gene, dpy-20, encodes a previously unknown type of protein, suggesting that there may be other classes of cuticle components still to be discovered and characterised mutationally. Here we describe two new dpy genes: dpy-31 and dpy-32.

Marie-Anne Felix et al. (2010) Evolutionary Biology of Caenorhabditis and Other Nematodes "Nodaviruses naturally infecting Caenorhabditis nematodes"

Eric Miska, Josephine Piffaretti, Guang Wu, David Wang, Alyson Ashe, Guoyan Zhao, Mabel Sanroman, Leonard Goldstein, Tony Belicard, Isabelle Nuez, Yanfang Jiang, Marie-Anne FELIX

[Evolutionary Biology of Caenorhabditis and Other Nematodes, 2010]

We found natural viral infections in wild isolates of both C. elegans and C. briggsae. The infections visibly affect the intestinal cells. Infected worm lysates passed through 0.2 um filters could be used to infect uninfected worms, which could be further passaged for many generations. Two highly divergent but related RNA viruses in the family Nodaviridae, tentatively named Orsay nodavirus and Santeuil nodavirus, were detected and sequenced. The viruses were subject to processing by the RNAi machinery as evidenced by the detection of virally derived small RNAs that mapped to the entire viral genome. These data demonstrate that nodaviruses are natural parasites of nematodes in the wild. We detect intra-specific variation in sensitivity to the virus among different C. elegans or C. briggsae isolates. Further study of the interactions between these viruses and nematodes is likely to provide insight into the natural ecology of nematodes and may reveal novel innate immune mechanisms that respond to viral infection.