Rummage, John et al. (2011) International Worm Meeting "A Website to Annotate SNP Data."

Barstead, Robert J., Miller, Kenneth G., Rummage, John

[International Worm Meeting, 2011]

The first step in analyzing whole genome sequence alignments is to detect variant sequences and associate them with genome annotations. Most genome sequence facilities have access to developers who run command line driven scripts to make this association. Our mission is to simplify this and make the annotation of SNP and Indel calls accessible to the average investigator. To this end we have launched Whole Genomes, a website where investigators can upload SNP-called files for custom annotations (http://seqreport.omrf.org/genome: open to all on May 1, 2011). Administratively, the site design is flexible, allowing one to easily create annotation tables based on tab delimitated flat files like the GFF files distributed by Wormbase. Further, the site uses simple forms to establish persistent templates that describe the format for uploaded SNP files. All files are imported into a MySQL database and all comparisons are done via MySQL queries that offer a much more dynamic interaction with the data compared to a simple script driven approach. Users do not need to know anything about annotation files, templates, or MySQL to use the site. Whole Genomes allows users to map SNPs to any combination of features in the annotation database, such as coding sequence, potential splice sites, untranslated regions, or microRNAs. For examples, a coding sequence query would report the specific amino acid changes for SNPs that fall within translatable sequence along with a metric of evolutionary conservation for that particular change. The site also allows the user to compare SNPs in two strains to identify both unique and common variations. In addition, if a user has minimal or no mapping information Whole Genomes can compare two allelic strains to find the gene that is affected in both. Each annotated SNP is associated with a unique "Download" link that lets users download the DNA sequence associated with the annotated feature. Finally, for any given SNP, the site will design PCR primers to isolate DNA for SNP verification.

Plenefisch JD et al. (1994) Worm Breeder's Gazette "Cloning mua-3: Some Observations on the New Molecular Era"

Plenefisch JD, Hedgecock EM

[Worm Breeder's Gazette, 1994]

Cloning mua-3: some observations on the new Molecular Era John Plenefisch and Edward Hedgecock, Dept. of Biology, Johns Hopkins University, Baltimore MD 21218

Parham C et al. (1994) Worm Breeder's Gazette "Tc4 and Tc5: What Makes Them Move and Why It Matters"

Beinhorn J, Collins JJ, Butze K, Parham C

[Worm Breeder's Gazette, 1994]

Tc4 and Tc5: what makes them move and why it matters Christi Parham, Kristie Butze, Joanna Beinhorn and John Collins. Dept. of Biochemistry and Molecular Biology, University of New Hampshire. Durham, NH 03824

Almeida CA et al. (1994) Worm Breeder's Gazette "Function of a Domain of the Myosin Heavy Chain Implicated in Familial Hypertrophic Cardiomyopathy"

Collins JJ, Almeida CA, Swift KE

[Worm Breeder's Gazette, 1994]

Function of a Domain of the Myosin Heavy Chain Implicated in Familial Hypertrophic Cardiomyopathy Craig A. Almeida, Kerry E. Swift and John J. Collins Department of Biochemistry and Molecular, University of New Hampshire, Durham, NH 03820

Chalfie M (1993) J Neurobiol "Touch receptor development and function in Caenorhabditis elegans."

Chalfie M

[J Neurobiol, 1993]

Mutations causing a touch-insensitive phenotype in the nematode Caenorhabditis elegans have been the basis of studies on the specification of neuronal cell fate, inherited neurodegeneration, and the molecular nature of mechanosensory transduction. (C) 1993 John Wiley & sons, Inc.

Maine EM et al. (1994) Worm Breeder's Gazette "Mutations That Enhance glp-1 Identify Genes Required For Various Aspects of Germline Development."

Gelber MB, Smardon AM, Shu P, Qiao L, Maine EM, Lissemore JL

[Worm Breeder's Gazette, 1994]

Mutations that enhance glp-1 identify genes required for various aspects of germline development. Eleanor Maine, Li Qiao, Jim Lissemore-, Pei Shu, Anne Smardon, and Melanie Gelber. Biology Dept., Syracuse University, Syracuse, NY 13244 and Biology Dept., John Carroll University, Cleveland, OH 44118.

Chalfie M (1998) Nature "Genome sequencing. The worm revealed."

Chalfie M

[Nature, 1998]

In 1983, John Sulston and Alan Coulson began to construct a complete physical map of the genome of the nematode worm Caenorhabditis elegans, and started what became known as the C. elegans Genome Project. At the time, several people wondered why John, who had just described all of the cell divisions in C. elegans (the cell lineage), was interested in this project rather than in a more 'biological' problem. He replied by joking that he had a "weakness for grandiose, meaningless projects". In 1989, as the physical map approached completion, the Genome Project, now including Bob Waterston and his group, embarked on the even more ambitious goal of obtaining the complete genomic sequence

Hotez PJ et al. (1993) Parasitol Today "Hookworm larval infectivity, arrest and amphiparatenesis: the Caenorhabditis elegans Daf-c paradigm."

Hotez PJ, Schad GA, Hawdon JM

[Parasitol Today, 1993]

Arrested development dramatically alters the life history of some species of soil-transmitted nematodes and elicits profound variations in the epidemiology of the infections they cause. Here, Peter Hotez, John Hawdon and Gerhard Schad show how an understanding of the cellular and molecular bases of arrested development may lead to new approaches for the control of ancylostomiasis and related infections.

Edgley, Mark et al. (2009) International Worm Meeting "C. elegans Gene Knockout Consortium Report: Progress, New Technologies and Funding."

Rummage, John, Edgley, Mark, Barstead, Bob, Flibotte, Stephane, Moerman, Don, Holmes, Jeff

[International Worm Meeting, 2009]

The C. elegans Gene Knockout Consortium (http://www.celeganskoconsortium.omrf.org/) has for many years pursued 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). Our primary approach uses a PCR detection method to generate single-gene deletions. More recently we have incorporated array Comparative Genome Hybridization (array-CGH; Genome Research 17: 337-347) and whole-genome sequencing for efficient detection of mutations. CGH has proven valuable and cost-effective for deletion discovery and SNP mapping (Genetics 181: 33-37; see abstract by Flibotte et al., this meeting). With deep sequencing we have generated the first comprehensive catalog of all mutations in a genetic background after EMS mutagenesis. The combined strategies of directed and non-directed approaches improve throughput, broaden the types of mutations we can identify, and in the long term should lower the cost per allele. All Consortium deletions are stabilized as homozygous or balanced heterozygous strains, 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 3,300 genes (not including about 700 genes deleted in natural isolates), and most of these have been stabilized and archived at the CGC. Together with those from the Mitani lab, deletion alleles represent over 5,000 genes. In the last two years we have been concentrating on genes encoding transcription factors and kinases, and we hope to complete the knockout coverage for these gene families in the next year. Of 934 total transcription factor genes, 720 are currently identified by gk, ok or tm deletions, with approximately another 50 identified by point mutation. Of 438 total kinase genes, 42 are represented by such deletions with another 150 identified by point mutation. Both our labs are currently in the process of renewing funding to continue this work. We plan to stay with the targeted PCR approach as funding allows, while continuing to develop CGH and deep sequencing and shifting resources to those methods as the technologies improve.

Waterston RH et al. J Neurogenet "John Sulston (1942-2018): a personal perspective."

Waterston RH, Moerman DG

[J Neurogenet]

John Sulston changed the way we do science, not once, but three times - initially with the complete cell lineage of the nematode <i>Caenorhabditis elegans</i>, next with completion of the genome sequences of the worm and human genomes and finally with his strong and active advocacy for open data sharing. His contributions were widely recognized and in 2002 he received the Nobel Prize in Physiology and Medicine.