Schwarz EM et al. (1996) East Coast Worm Meeting "Cellular and molecular analysis of thermosensation"

Chalfie M, Schwarz EM

[East Coast Worm Meeting, 1996]

While senses like sight, hearing, and mechanosensation are becoming well understood, thermosensation remains obscure. Work by Hedgecock (1) and Mori (2) has shown that C. elegans is a promising model system for metazoan thermosensation, but neither the cells nor the genes required for thermosensation in C. elegans are fully known. Previous work in this laboratory (3) has shown that at least three new deg mutations cause cells in the head to degenerate while partially crippling thermosensation; none of these are allelic to previously described ttx mutations . We have therefore begun to determine which cells are defective in these deg mutations. We have also begun genetic mapping experiments aimed at positional cloning of the wild-type deg loci. References: 1. Hedgecock, E.M. and Russell, R.L. (1975). Proc. Natl. Acad. Sci. U.S.A. 72, 4061-4065. 2. Mori, I. and Ohshima, Y. (1995). Nature 376, 344-348. 3. Treinin, M. and Chalfie, M. (1993). International C. elegans meeting abstracts, p. 446.

Hobert O (2010) Neuronal Development, Synaptic Function and Behavior, Madison, WI "Terminal selectors: how the worm builds its nervous system"

Hobert O

[Neuronal Development, Synaptic Function and Behavior, Madison, WI, 2010]

One of the central questions in developmental neurobiology is how a developing organism can generate a vast array of distinct neuronal cell types. For a terminally differentiating neuron this questions boils down to a gene regulatory problem that necessitates the decoding of the regulatory programs that instruct neurons to turn on neuron type-specific gene expression programs. Through the decoding of cis-regulatory elements and forward genetic screen in C.elegans, my laboratory has begun to uncover what appears to some simple, phylogenetically conserved principles that may underlie the generation of neuronal diversity that I will describe in this talk.

Pungaliya, Chirag et al. (2009) International Worm Meeting "Systematic identification of steroids in Caenorhabditis elegans."

Pungaliya, Chirag, Wollam, Joshua, Antebi, Adam, Seim, Kristen, Schroeder, Frank, Malik, Rabia, Bethke, Axel

[International Worm Meeting, 2009]

Recently Motola et. al. identified the dafachronic acids, bile-acid like steroids that act as the endogenous ligands of the nuclear hormone receptor DAF-12. They directly bind to DAF-12 to influence interactions with its cofactors and thereby regulate transcriptional activity. It is possible that other endogenous steroids influence DAF-12 or act on other nuclear hormone receptors that modulate various C. elegans life history traits. We have begun a systematic analysis of C. elegans steroid metabolism based on chromatographic separation, bioassays and differential analysis by 2D NMR spectroscopy (DANS), comparing the wild-type metabolome to that of mutants with suspected defects in steroid metabolism. So far our investigations have revealed several steroids whose presence in C. elegans had not previously been recognized.

Robert P Johnson et al. (2002) Mid-west Worm Meeting "The dystroglycan-like protein DGN-1 is required for multiple epithelial and neural functions."

Seong Hoon Kang, Robert P Johnson, James M Kramer

[Mid-west Worm Meeting, 2002]

The vertebrate protein dystroglycan provides a transmembrane linkage between basement membrane components and intracellular signaling and cytoskeletal networks. While research has focused on the function of dystroglycan in muscle, the wide expression of the protein in epithelial and neural tissue suggests important roles in mediating cell-ECM interactions in other cell types. Three predicted genes in C. elegans show sequence similarity to dystroglycan. Based on comparison of amino acid sequence and domain organization of the predicted products, the most similar of these is dgn-1 (LG X, T21B6.1). We have begun to characterize the protein product and biological roles of dgn-1.

Wilkinson HA et al. (1991) International C. elegans Meeting "1991 LIN-12 UPDATE."

Kao G, Greenwald IS, Grant BD, Yochem JJ, Wilkinson HA, Fitzgerald K

[International C. elegans Meeting, 1991]

On this poster, we will report on our progress in a number of studies of lin-12 and associated genes that will not be covered in other presentations from our laboratory. In particular, we are currently examining transformed lines containing various lin-12--1acZ fusion constructs and generating monoclonal and anti-peptide antisera in order to characterize the expression and distribution of l in- 12 mRNA and protein products. We have also begun to clone certain sel genes and to construct a full-length lin-12 cDNA for various manipulations. We will also report on the various EGFrelated genes that we have isolated using lin-12 and glpI probes.

Chung, George et al. (2013) International Worm Meeting "CHL-1 is required for DNA replicative integrity in Caenorhabditis elegans."

Rose, Ann M, Chung, George

[International Worm Meeting, 2013]

Previously, we have described chl-1 in C. elegans, an ortholog of the human DDX11/ChlR1 gene associated with Warsaw breakage syndrome. Our published results have shown that CHL-1 is indispensable for cell proliferation and for genome integrity. Using the continuously-replicating, mitotic nuclei of the C. elegans germline, we have begun to assay the recruitment of repair factors to the DNA under various non-damaging and damaging conditions. Even in the absence of DNA damaging agents, the chl-1 mutant DNA is marked by an abnormally high number of RAD-51 foci, indicating that the CHL-1 protein is required for the normal, breakage-free completion of mitotic replication.

Petcherski AG et al. (1997) International C. elegans Meeting "IS SNO IMPORTANT FOR GLP-1/LIN-12 SIGNALING IN C. elegans?"

Petcherski AG, Henderson ST, Kimble JE, Banerjee U

[International C. elegans Meeting, 1997]

In Drosophila, strawberry Notch (sno) is involved in inductive interactions mediated by Notch (A. Majumdar & U. Banerjee, submitted). To address a possible function of sno in worms, we have cloned the C. elegans homolog, called Ce-sno, and begun to characterize its role in development. Injection of anti-sense RNA generates sterile progeny with fewer than normal germline cells and defective gametogenesis. The injections do not generate either dead embryos or Lag larvae. Given the role of sno in Notch-mediated inductive interactions in Drosophila, it is tempting to speculate that Ce-sno may be required for induction by GLP-1. Progress on the further characterization of this locus will be presented.

Sabrina G C Shore et al. (2002) West Coast Worm Meeting "The temperature sensitive lethal mutation or566 may define a new gene that functions in early morphogenesis"

Andrew D Chisholm, Sarah L Moseley, Sabrina G C Shore

[West Coast Worm Meeting, 2002]

Mutations in the EPH receptor tyrosine kinase VAB1 and in its ephrin ligands cause incompletely penetrant defects in gastrulation cleft closure and epidermal enclosure. Fully penetrant defects in cleft closure are seen when multiple pathways are blocked (e.g. vab-1 and ptp-3 (Harrington et al., 2002, Development 129: 2141). To find genes that may have essential functions in gastrulation cleft closure we have begun to examine conditional lethal mutants for possible defects in this process. Bruce Bowermans lab identified several new temperature-sensitive (ts)-lethal mutations affecting morphogenesis in their large scale ts-lethal screens, and very kindly provided some of them to us.

Kalb JM et al. (1997) International C. elegans Meeting "FKH-1 IS EXPRESSED IN THE PHARYNX, RECTUM AND SOMATIC GONAD"

Kalb JM, McGhee JD, Goszczynski B, Lau KK

[International C. elegans Meeting, 1997]

C. elegans fkh-1 is a member of the fork head/HNF-3 family of transcription factors. We have raised antibodies to a portion of FKH-1 common to the products of all three major fkh-1 transcripts. These antibodies react with most (possibly all) nuclei of the embryonic pharynx and eight nuclei in the rectal region. If FKH-1 protein can be detected at all in the intestine, it is transitory: this agrees with our previous in situ hybridization results. However, reporter constructs (with 7 kb of upstream DNA) express heavily in the gut, suggesting additional control elements must exist. FKH-1 remains detectable in the pharynx and rectum at all larval stages. We have begun to examine fkh-1 expression in mutants with abnormal pharynx development. FKH-1 appears to be expressed normally in pha-1 (e2123ts) embryos but can not be detected in pha-4 (q490) embryos. fkh-1 maps near pha-4 and the expression pattern of fkh-1 matches what one might expect the expression pattern of pha-4 to be (Susan Mango, personal communication), raising the possibility that fkh-1 and pha-4 may indeed be the same gene. FKH-1 antibodies also react with nuclei in larval distal tip cells and ventral uterine cells. Interestingly, a fkh-1::lacZ reporter fusion, which is also expressed in the somatic gonad, is not expressed in the somatic gonad of lin-15 (e1763) animals. We have begun to look at fkh-1 somatic gonad expression in other mutants in vulva and uterine development.

Powell J R et al. (2010) Aging, Metabolism, Stress, Pathogenesis, and Small RNAs, Madison, WI "Transcriptional Targets of the G-Protein Coupled Receptor FSHR-1"

Powell J R, Ausubel F M, Anthony H L, Hibshman J D

[Aging, Metabolism, Stress, Pathogenesis, and Small RNAs, Madison, WI, 2010]

Innate defense responses to infection by pathogenic microorganisms are both ancient and critical for the survival of vertebrates and invertebrates. To trigger a defense response, a multicellular host employs specific receptors to detect the presence of a pathogen or the damage caused by infection by that pathogen. The G-protein coupled receptor FSHR-1 is hypothesized to be one such receptor in C. elegans. We have previously shown that FSHR-1 is required for the innate immune response to intestinal infection by diverse pathogens. FSHR-1 signals in parallel to known defense pathways and regulates a set of early infection response genes. We have performed a microarray analysis to identify all the transcriptional targets of FSHR-1 and have begun to characterize those genes that appear to be regulated by FSHR-1 in response to infection.