Mains PE (1994) Worm Breeder's Gazette "Interactions Between mei-1 and the unc-116 Kinesin"

Mains PE

[Worm Breeder's Gazette, 1994]

Interactions Between mei-l and the unc-116 Kinesin Paul E. Mains, Dept. of Medical Biochemistry, University of Calgary, Calgary, Alberta, Canada

Wissmann AK et al. (1994) Worm Breeder's Gazette "Characterization of the let-502 Gene"

Mains PE, Wissmann AK, McGhee JD

[Worm Breeder's Gazette, 1994]

Characterization of the let-502 gene Andreas Wissmann, James D. McGhee and Paul E. Mains, Dept. of Medical Biochemistry, University of Calgary, Calgary, Alberta, Canada T2N 4N1

Sommer RJ et al. (1994) Worm Breeder's Gazette "Evolution of Vulva-Formation: Part II: Species With a Central Vulva"

Sommer RJ, Sternberg PW

[Worm Breeder's Gazette, 1994]

Evolution of vulva-formation: Part II: Species with a central vulva Ralf J. Sommer & Paul W. Sternberg, California Institute of Technology, Division of Biology 156-29, Pasadena, CA 91125

Li WQ et al. (1992) Worm Breeder's Gazette "Characterization of the Axonal Guidance and Outgrowth gene Unc-33"

Shaw JE, Li WQ, Herman RK

[Worm Breeder's Gazette, 1992]

Characterization of the axonal guidance and outgrowth gene unc-33 W. Li, R. K. Herman and J. E. Shaw Department of Genetics and Cell biology, University of Minnesota, St Paul, MN 55108

Sommer RJ et al. (1994) Worm Breeder's Gazette "Evolution of Vulva Formation: Part IV: Variation in AC Position Can Cause a Shift of Vulva Formation Towards P(4-6).p."

Sternberg PW, Sommer RJ

[Worm Breeder's Gazette, 1994]

Evolution of vulva formation: Part IV: Variation in AC position can cause a shift of vulva formation towards p(4- 6).p Ralf J. Sommer & Paul W. Sternberg, HHMI & California Institute of Technology, Division of Biology 156-29, Pasadena, CA

Scott Alper et al. (2005) International Worm Meeting "Development of two high-throughput RNA-interference assays to investigate innate immunity"

David Schwartz, Jonathan H Freedman, Paul Dunlap, Scott Alper

[International Worm Meeting, 2005]

In response to infection, humans mount an immediate innate immune response as well as a slower but more specific adaptive immune response. The immediate response involves secretion of antimicrobial compounds and infiltration of cytotoxic and phagocytic cells at the site of infection. While innate immunity plays a vital role in pathogen defense, misregulation of innate immunity also plays a role in the onset of many human diseases including sepsis, asthma, atherosclerosis, and organ rejection. To investigate the genetics of innate immunity, we are using both C. elegans and mammalian tissue culture as model systems. Our lab has identified many candidate mouse innate immunity genes using DNA microarrays and QTL analysis. We are now developing two high throughput assays to determine the function of these genes. Both assays use RNA-interference to inhibit gene function. One assay uses the nematode C. elegans as a model system. In response to infection with a pathogen, C. elegans produces antimicrobial compounds as part of its innate immune response. We have engineered gfp fusions to antimicrobial genes induced by infection with Serratia marcescens or Staphylococcus aureus. Using RNAi, we are currently inhibiting C. elegans orthologs of candidate innate immunity genes to determine their effect on antimicrobial gene expression. Genes identified in this primary screen are then rescreened in assays to monitor C. elegans pathogen load and pathogen-mediated toxicity. In the other assay, mouse macrophages are treated with lipopolysaccharide (LPS) and cytokine production is measured. Using siRNAs to inhibit gene function, we are beginning to test the effect of candidate genes on cytokine production. In preliminary experiments, we have identified several novel genes that are required for production of TNF-alpha and IL-6. Using these two assays, we hope to rapidly identify and determine the function of candidate innate immunity genes.

Scott Alper et al. (2008) C.elegans Aging, Stress, Pathogenesis, and Heterochrony Meeting "Novel Innate Immunity Gene and Pathway Discovery Using Comparative Genomics"

Paul Dunlap, Jonathan Freedman, Windy Boyd, Brad Lackford, Scott Alper, David Schwartz, Rebecca Laws

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

In response to infection, humans mount an immediate innate immune response and a slower but more specific adaptive immune response. The innate response involves the action of phagocytic and cytotoxic cells that fight the infection. Therefore, the innate immune system plays a vital role in host defense. However mis-regulation of innate immunity can also contribute to a variety of immunological diseases, including asthma and sepsis. Thus, the identification of genes that regulate innate immunity is critical to understanding host defense and to identifying potential targets for treatment of infectious and immunological diseases. While many genes that regulate the response to Gram negative lipopolysaccharide (LPS) have been discovered, it is unclear how many other genes regulate this response. To identify novel regulators of the innate immune response to LPS (and other microbial toxins), we developed assays in two model systems to inhibit candidate genes by RNA-interference and monitor the subsequent immune response. Both models utilize a Gram negative bacterial stimulus. In one in vivo assay, the nematode C. elegans was stimulated with E. coli and production of antimicrobial proteins was monitored. In the second in vitro assay, mouse macrophages were stimulated with LPS and cytokine production was monitored. Genes that altered innate immune responsiveness in these systems were validated using mutant nematode models and are currently being tested in mutant murine models. These assays have led to the discovery of 11 genes that regulate the innate immune response in both systems and the identification of a novel protein interaction network with a conserved role in innate immunity regulation. These genes represent potential therapeutic targets for infectious and immunological diseases.

Paul Sternberg (2002) Worm Breeder's Gazette "Position at Caltech, CA"

Paul Sternberg

[Worm Breeder's Gazette, 2002]

CURATOR. Will annotate gene functions in C. elegans , using Gene Ontology (Nature Genetics [2000], vol. 25, pp. 25-29). Duties include: analysing gene functions in the primary literature; judging the optimal description of these functions in Gene Ontology, inventing new terms for Gene Ontology where necessary; and incorporating these descriptions into Wormbase. A Ph.D. in some area of biology and substantial C. elegans experience are required. The successful job candidate will have broad scientific erudition, verbal articulacy, and creative intelligence as well as patience and a willingness to work hard. Computer literacy in UNIX or Linux is a plus, but is not required. Direct inquiries to Paul Sternberg (pws@its.caltech.edu).

Theresa Stiernagle et al. (1992) Worm Breeder's Gazette "The Caenorhabditis Genetics Center (CGC) Has Moved"

Bob Herman, Theresa Stiernagle, Jonathan Hodgkin

[Worm Breeder's Gazette, 1992]

On July 19, 1992 Mark Edgley arrived on the University of Minnesota campus in a rented truck containing frozen worms, computer and files. Mark stayed in St. Paul for two weeks to help us get organized and operational. We are extremely grateful to Mark and Don Riddle for the splendid way they have prepared for this transition. We shall try to continue the excellent tradition of CGC service they have established (pause for prolonged applause for Mark and Don). Jonathan has taken over responsibility for the genetic map. Genetic map data for new genes, improved locations for known genes, and new data on rearrangements (duplications, deficiencies, balancers, and so on) should all be sent Cambridge UK (or St. Paul, MN for forwarding to Cambridge), using standard formats. Forms are available on request. In order to improve the correlation between the genetic and physical maps, the CGC also wishes to collect published and unpublished genetic map data for genes, sequences and RFLP's with defined positions on the physical map. Data should be sent to Cambridge UK or St. Paul, MN, using (as far as possible) the standard genetic map data formats, as above. We also encourage submission of genetic map data by e-mail. Investigators who wish to use this option should send a message to jah@mrc-lmb.cam.ac.uk. What follows are reminders of additional ways in which you can help us: 1. Please try to remember to acknowledge in papers the use of any strains received from the CGC. 2. Please send us reprints of au of your papers; if a paper acknowledges the CGC, we would be happy to receive two reprints, because we must send one to NIH. 3. Please let us know if you find a bibliographic reference we have missed (particularly if it is one of your own). 4. Our first priority in acquiring strains is to acquire a reference allele of every identified gene and all available chromosome rearrangements. If you can help us fill gaps in our collection without our asking, all the better. 5. We need your strain requests in writing (e-mail is fine), with a brief statement of research or training activity for which the strains are intended.

Emmons SW (1997) Trends Genet "Worms as an evolutionary model."

Emmons SW

[Trends Genet, 1997]

Focused studies on model organisms with favorable features have been important for advancing many areas of biology. Nematodes have been a successful model for analyzing development. Can they also be used to study evolution? Paul Sternberg and his present and former colleagues are attempting to answer this question by studying variation of that well-described little structure, the nematode vulva. Their efforts have been well rewarded. Two recent publications extend a series of papers showing a surprising degree of evolutionary variability in vulval development among species. Could it be that comparison of nematode species will prove to be as powerful for penetrating the intimate mechanisms of evolutionary change as analysis of mutant nematodes has been to understanding mechanisms of development?