Miller DM et al. (1992) Worm Breeder's Gazette "unc-4 LacZ Expression in A-Type Motor Neurons"

Miller DM, Niemeyer CJ

[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

Kitamura S et al. (1994) Worm Breeder's Gazette "The Troponin C Gene, tnc-1, of Caenorhabditis elegans: Genome Structure and Mutation Sites of pat-10"

Williams BD, Kitamura S, Kagawa H, Sakube Y, Matsumoto S

[Worm Breeder's Gazette, 1994]

The troponin C gene, tnc-1 of Caenorhabditis elegans: Genome structure and mutation sites of pat-10 S. KITAMURA, B. WILLIAMS*, Y. SAKUBE, S. MATSUMOTO and H. KAGAWA, Dept. of Biol., Fac. of Sci., Okayama University, Japan, 700. *;Dept. of Gen., Washington Univ. School of Med., St. Louis

Ali Khan L et al. (1994) Worm Breeder's Gazette "cej-1 Encodes a Novel Protein With Poly-Threonine Motif"

Siddiqui SS, Fukushige T, Ali Khan L, Tsukita Sh, Tabish M, Itoh M

[Worm Breeder's Gazette, 1994]

cej-1 Encodes a Novel Protein with Poly-Threonine Motif M. L. A. Khanl, M. Tabish, T. Fukushigel1 S. Tsukita2, M. Itoh , Sh. Tsukita , and S. S. Siddiqui. (1): Lab. of Molecular Biology, Dept of Ecological Engg. Toyohashi Univ. Technology, Toyohashi 441, and (2). National Institute for Physiological Sciences, Okazaki 444, Japan.

Salser SJ et al. (1994) Worm Breeder's Gazette "mab-5 Expression Repeatedly Switches ON and OFF in the V5 Lineage"

Kenyon CJ, Salser SJ

[Worm Breeder's Gazette, 1994]

mab-5 Expression Repeatedly Switches ON and OFF in the V5 Lineage S. Salser and C. Kenvon, UCSF, San Francisco, CA. 94143

Link CD (1995) Worm Breeder's Gazette "Modulation of Amyloid Formation in Transgenic Worms."

Link CD

[Worm Breeder's Gazette, 1995]

Modulation of amyloid formation in transgenic worms. Chris Link Dept. of Biology, University of Denver, Denver, CO 80208 Although the identification of germline mutations in the amyloid precursor protein (APP) gene in some familial cases of Alzheimer's Disease has provided compelling evidence for a central role of b-amyloid in this disease, in the vast majority of cases no primary sequence changes are found. Because a number of lines of evidence suggest that the conversion of b-peptide (the initial proteolytic product of the APP gene) into insoluble, fibrillar b- amyloid is critical for the pathological effects of this protein, much recent work has focused on the mechanisms in the brain that enhance or inhibit this process. In vitro studies have demonstrated that some proteins (e.g., apolipoprotein E, anti-chymotrypsin) can enhance the formation of insoluble b- amyloid, while others ( e.g., transthyretin) can inhibit its formation. As described previously, I have constructed transgenic worms that express human peptide under control of the unc-54 promoter. These animals have muscle-specific anti-b immunoreactive deposits that bind the amyloid-specific dye thioflavine S. The dye reactivity of these deposits is particularly interesting, because it implies that the expressed b- peptide is forming insoluble amyloid deposits (something that has not yet been reported for transgenic mouse models). To determine if the in vitro amyloid-inhibiting effects of transthyretin can be observed in vivo, I have generated transgenic animals co-expressing b- peptide and transthyretin in muscle cells. This was accomplished by mating an inregrated unc-54/transthyretin transgenic strain to integrated unc-54 / b-1-42 transgenic strains, and dye-staining the resultant double transgene heterozygotes. These animals have greatly reduced (<15percent) numbers of dye-reactive deposits (compared to single transgene heterozygous controls), suggesting that transthyretin is inhibiting b- amyloid formation in this in vivo model. (Unfortunately, I have been unable to maintain double homozygous lines.) A trivial explanation for this result is that coexpression of the two transgenes simply reduces the amount of b- peptide made, which in turn reduces the number of deposits. Although the pattern of anti-transthyretin and anti-b- staining in these animals is indistinguishable from that of the respective singly transgenic animals, immunohistochemistry is probably not quantititative enough to rule out this trivial explanation. Transthyretin variants that fail to inhibit b- amyloid formation have recently been reported; repeating this experiment with such variants will presumably be a good control. It will also be interesting to see if the opposite result can be obtained co- expressing the "pathological chaperones" that may enhance b- amyloid formation.

Rosenberg R (1978) Worm Breeder's Gazette

Rosenberg R

[Worm Breeder's Gazette, 1978]

All eyes are on the newest fashion trend, the Dumpy Look . Pace setting designer I.M. Worm s androgynous wardrobe is all the rage in Paris. Bianca Jagger quips, Tres, tres - Women s Wear Daily writes, Elegans personified - Patti Smith thinks, The punks won t buy it and Craig Russell says, It fits right in with my act . A product of Mutant Isolation, Inc.

Musset-Bilal F et al. (1994) Worm Breeder's Gazette "Characterization of the C. elegans Basement Membrane-Associated Protein SPARC"

Musset-Bilal F, Schwarzbauer JE, Ryan CS

[Worm Breeder's Gazette, 1994]

Characterization of the C. elegans Basement Membrane- Associated Frederique Musset-Bilal, Carol S. Ryan, and Jean E. Schwarzbauer Department of Molecular Biology, Princeton University, Princeton NJ 08544

Simske JS et al. (1994) Worm Breeder's Gazette "Specification of Vulval Cell Fates By Sequential Signalling Pathways."

Simske JS, Kim SK

[Worm Breeder's Gazette, 1994]

Specification of vulval cell fates by sequential signaling pathways Jeffrey S. Simske and Stuart K. Kim, Dept. of Developmental Biology, Stanford University Medical Center, Stanford CA 94305

Richards JP et al. (1991) Worm Breeder's Gazette "The Cloning of a Putative C. elegans Cyclin B Gene Using the Polymerase Chain Reaction."

Bennett KL, Richards JP, Temenak JJ

[Worm Breeder's Gazette, 1991]

Cyclin proteins are intimately involved in cell cycle regulation. Two types of cyclin proteins have been identified, cyclin A and cyclin B. The cyclin A protein has been shown to be critical to embryonic development in Drosophila; homozygous mutant embryos lacking cyclin A die when zygotic transcription fails to provide cyclin A. The presence of cyclin B protein cannot rescue these mutants (C.F. Lehner and P.H. O'Farrell, Cell 1990. 61:535-547). No mutants in cyclin B have been reported in Drosophila. Cyclin B protein has been shown to be involved in meiotic maturation in clams (Westendorf et al., J. Cell Biol. 1989. 108:1431-1444). Perhaps surprisingly, in Drosophila the mRNA for cyclin B localizes by in situ hybridization to the Drosophila pole cells, the fly equivalents of the nematode P germline cell lineage (Whitfield et al., Nature 1989. 338:337340). The Bennett laboratory is interested in the nematode germline lineage and in identifying the components of the germline P granules ( Strome and Wood, Cell 1983. 35:15-25 and K. Bennett, WBG 9:1 55). We plan to determine if nematode cyclin B RNA is similarly localized to the nematode germline precursor cells, and would like to address what possible role the sequestration of cyclin B RNA plays in the determination of the germline. Using primers to conserved cyclin B regions, we have isolated, cloned and sequenced a PCR product from genomic Caenorhabditis DNA which is a putative cyclin B. As illustrated below, this fragment has 72% exact match at the amino acid level to the corresponding region of the clam or sea urchin cyclin B genes; this is exactly the same match ( 41/57 aa) that sea urchin and clam show to each other in this region. Southern blot analysis using this fragment as a probe with C. elegans DNA indicates a single copy gene. The PCR fragment recognizes a single 1.4 kb message on Northern analysis using polyA+ RNA from mixed stage worms; this size is large enough to accommodate the coding region of the cyclin B protein. We have recently screened R. Barstead's lambda ZAP mixed stage cDNA library. Thirty putative cyclin B cDNAs were detected on duplicate lifts when 120,000 phage were screened. [See Figure 1]

Miller LM et al. (1998) Worm Breeder's Gazette "The Effects of Benzo[a]pyrene (cough cough!) on C. elegans"

Miller LM, Hartman PS

[Worm Breeder's Gazette, 1998]

The polycyclic aromatic hydrocarbon (PAH) benzo[a]pyrene (B[a]P) is a major carcinogenic component of cigarette smoke and many other combustibles. Wild-type (N2) and four radiation hypersensitive mutants (rad-1, rad-2, rad-3 and rad-7) were exposed to different B[a]P concentrations for either one or 24 hours. Survivorship curves were generated for both embryos and L1s. In addition, hermaphrodites were exposed to B[a]P and the effects on brood sizes were measured. Relative to most studies, very high B[a]P concentrations were required to significantly reduce survival or brood sizes in C. elegans. All strains showed greater sensitivity with longer exposure. Surprisingly, the rad mutants were no more sensitive than wild type. Since no recessive lethal mutations were detected in the 500 plates screened using the eT1 balancer system, B[a]P does not readily induce mutations in C. elegans. Finally, using a specific and sensitive RIA, no adducts were detected in C. elegans DNA extracted from animals exposed to high B[a]P concentrations. The extreme resistance of C. elegans is likely due to the failure of this nematode to metabolize B[a]P into more toxic and mutagenic compounds.