Boeck, Max E. et al. (2009) International Worm Meeting "Predicted 3D Structures of the DNA-Binding Domain for the Ten C. elegans GATA Transcription Factors and Their Preferred DNA Sequence."

Waterston, Robert, Thompson, James, Bradley, Phil, Boeck, Max E.

[International Worm Meeting, 2009]

Based on the paradigm that structure dictates function we used a computational approach to determine the preferred DNA motif bound by each of the GATA transcription factors found in C. elegans. GATA transcription factors have been shown to be important for organogenesis and cell fate specification in every metazoan from C. elegans to humans. The ability of GATA factors to specify cell-fate decisions is dictated by their ability to bind a DNA motif, WGATAR, with high fidelity. GATA factors have been shown to bind the motif through the actions of a conserved DNA-binding structure, CXXC(X)17-19CXXC [1]. While the basic DNA-binding structure is conserved between members of the GATA family,numerous specificity-determining residues vary between GATA genes. Using a maximum-likelihood phylogenetic approach [2] we estimated a phylogenetic tree in order to model the evolutionary relationships between GATA factors in the sequenced Caenorhabditis species. We then used Rosetta homology modeling [3] to construct structural models of the DNA-binding structures of all the GATA factors found within C. elegans. By tracking the specificity-determining residues that have changed along the phylogenetic tree of these GATA factors, we have defined a prediction of which GATA factors are likely to bind very similar segments of DNA. [1] Lowry, Atchley J Mol Evol. 2000 50:103-115 [2] Guindon S, Gascuel O. Syst Bio. 2003 52(5):696-704. [3] Qian et al, Nature. 2007 Nov 8;450(7167):259-64.

Larson SD et al. (2018) Philos Trans R Soc Lond B Biol Sci "Connectome to behaviour: modelling Caenorhabditis elegans at cellular resolution."

Gleeson P, Larson SD, Brown AEX

[Philos Trans R Soc Lond B Biol Sci, 2018]

It has been 30 years since the 'mind of the worm' was published in <i>Philosophical Transactions B</i> (White <i>et al</i> 1986 <i>Phil. Trans. R. Soc. Lond. B</i><b>314</b>, 1-340). Predicting <i>Caenorhabditis elegans</i>' behaviour from its wiring diagram has been an enduring challenge since then. This special theme issue of <i>Philosophical Transactions B</i> combines research from neuroscientists, physicists, mathematicians and engineers to discuss advances in neural activity imaging, behaviour quantification and multiscale simulations, and how they are bringing the goal of whole-animal modelling at cellular resolution within reach.This article is part of a discussion meeting issue 'Connectome to behaviour: modelling <i>C. elegans</i> at cellular resolution'.

Sengupta P et al. (2014) Traffic "New insights into an old organelle: meeting report on biology of cilia and flagella."

Barr MM, Sengupta P

[Traffic, 2014]

The rising interest of the scientific community in cilia biology was evident from the fact that registration for the third FASEB conference on 'The Biology of Cilia and Flagella' closed out before the early bird deadline. Cilia and flagella are organelles of profound medical importance; defects in their structure or function result in a plethora of human diseases called ciliopathies. 240 clinicians and basic scientists from around the world gathered from 23 June 2013 to 28 June 2013 at Sheraton at the Falls, Niagara Falls, NY to present and discuss their research on this intensely studied subcellular structure. The meeting was organized by Gregory Pazour (University of Massachusetts Medical School), Bradley Yoder (University of Alabama-Birmingham), and Maureen Barr (Rutgers University) and was sponsored by the Federation of American Societies for Experimental Biology (FASEB). Here, we report highlights, points of discussion, and emerging themes from this exciting meeting.

Hodgkin JA (1988) Worm Breeder's Gazette "informational suppression by male-abnormal mutations: new names, new data."

Hodgkin JA

[Worm Breeder's Gazette, 1988]

As previously reported (WBG 10-1: 112, 10-2: 30, etc.) mutations at six different loci act as allele-specific suppressors of mutations in a variety of genes: tra-2, unc-54, etc. These mutations also have characteristic morphological effects on the anatomy of the adult male tail and, to a lesser extent, of the hermaphrodite vulva. For this reason they have hitherto been assigned to the mab (male abnormal) gene category: mab-1, ed) and mab-12 through mab-16 (unpublished). However, they exhibit such a distinctive set of common properties that it has been decided (with the agreement of Andy Papp, Victor Ambros, Rock Pulak and Phil Anderson, who have been responsible for isolating most of these suppressor mutations) to assign them to a new gene

K Kawamura et al. (1999) International C. elegans Meeting "Structure of Neural Network of C. elegans Observed by a Random Walker"

Y Osana, K Kawamura, K Oka, K Oshio, Y Funabashi, S Morita

[International C. elegans Meeting, 1999]

A database of synaptic connectivity of 302 neurons of the C. elegans has been constructed[1] from the observations of Albertson and Thomson[2] and White et al.[3] by some of the present authors. A network formed by 302 neurons of the C. elegans is represented on a computer by a network which consists of 302 dots combined by (arrowed) bonds. To analyse the structure of the neural network, behavior of a random walker on it is studied. The walker is displaced among dots which represent neurons over bonds which model synaptic connection. In terms of walking distance defined by minimum time steps which is necessary for the random walker to be displaced between neurons, distances among all neurons, whose synaptic connectivity are described by the above authors, have been determined. Almost all neurons are located within the walking distance of three time steps but walking distance among phalingeal neurons and somatic neurons are more than four time steps. The network is extended in a (more than) nine dimensional space around three nanohedra which are mutually combined by manifolds of less dimension. Each nanohedron consists of nine dots representing interneurons mutually connected by synapses and these nanohedra are located near the center of the network. The lattice is biased by the rectification of the chemical synapse in the sence that a random walker prefers to be displaced from sensory neurons to motor neurons. [1] K. Oshio, S. Morita, Y. Osana and K. Oka: C. elegans connectivity data, Technical report of CCEP, Keio Future No.1 (1998) [2] D. G. Albertson and J. N. Thomson: Phil. Trans R. Soc. Lond. B. 275 (1976) 299 [3] J. G. White, E. Southgate, J. N. Thomson and S. Brenner: Phil. Trans. R. Soc. Lond. B 314 (1986) 1.

Barbazuk BW et al. (1995) Worm Breeder's Gazette "Correlation of the Genetic and Physical Maps Within the rol-3 Region of LGV (left)."

Baillie DL, Barbazuk BW

[Worm Breeder's Gazette, 1995]

Correlation of the Genetic and Phvsical maps within the rol-3 region of LGV (left) W. Bradley Barbazuk and David L. Baillie Institute of Molecular Biology and Biochemistry, Simon Fraser University, Burnaby, BC. CANADA, VSA 1 S6 In an attempt to identify the physical location of the rol-3 (V) gene we have begun the systematic germ-line transformation rescue of lethal mutations within zones 16-18 of LGV (JOHNSEN and BAILLIE, GENETICS 129: 735-?52). Using H. Kagawa's placement of unc-68 (WBG 12(4)) as a starting point we began to inject cosmids to the right of C46C6 into N2 hermaphrodites. In doing so we were able to obtain a battery of strains each carrying cosmids singly, or multiply, in stable arrays which were then used as mini-duplications in subsequent crosses to lethal bearing strains. In total we used eight cosmid bearing strains and one YAC bearing strain in the rescue of 13 lethal mutations including rol-3 (Table 1). Our germ-line transformation rescue data has enabled us to split up and order some of the lethal mutations within the zone 16-18 gene clusters. (Figure 1). We would like to thank C. Mello and J. Priess for providing a strain carrying an array composed of ZK307, F25G6 and FOlH8, as well as providing purified DNA for many of the cosmids injected.

Casson LP et al. (1986) Worm Breeder's Gazette "effects of duplicating X-linked genes on the general expression of the Xchromosome."

Meyer BJ, Casson LP

[Worm Breeder's Gazette, 1986]

mnDp10 is a large duplication of the right side of X, covering the myo-2 gene. Northern assays indicate that an XX hermaphrodite carrying two copies of mnDp10 accumulates twice as much myo-2 mRNA as a wild-type hermaphrodite. This observation indicates that expression of the myo-2 gene is in proportion to its copy number, an important control for our dosage compensation experiments. In examining three other X-linked loci not covered by this duplication, we discovered that the two dosage compensated loci, uxt-1 (adjacent to sup-7) and uvt-4 (adjacent to the vit genes) are also affected by this duplication. The levels of uxt-1 and uvt-4 mRNA are twice as high in the duplication strain as in a wildtype hermaphrodite strain. However, act-4 expression remains unchanged by mnDp10. (Expression of uxt-1 and uvt-4 is elevated in dpy-21, dpy27, dpy-28, and egl-16 strains whereas expression of act-4 is not). We are currently investigating the relevance of these observations to the mechanism of dosage compensation. (Phil Meneely has observed a similar phenomenon: lin-15 hypomorphs are suppressed by X duplications not covering this locus.)

German EA et al. (1998) East Coast Worm Meeting "CROSSED WIRES IN UNC-37 VENTRAL CORD"

Hall DH, Miller DM, German EA

[East Coast Worm Meeting, 1998]

Uncoordinated movement in unc-37 adults is superficially similar to the impairment observed in unc-4 animals (1). In unc-4, loss of coordination results from a specific wiring deficit between interneurons and motorneurons in the ventral nerve cord (3,4). We are currently analyzing the detailed synaptic pattern in an adult unc-37 nerve cord from serial thin sections. Preliminary data were discussed previously (2). We have now identified the major interneurons and 20 motorneurons in the anterior ventral nerve cord, and have determined their synaptic interactions. The morphological phenotype of unc-37 is not as limited as the specific wiring defect in unc-4. Many neurons show minor changes in branching or axon caliber, and there is a wider variety of wiring changes. However, in both mutations the AVB interneurons form inappropriate gap junctions onto class A targets, while AVAs fail to make normal junctions onto these targets. This specific change may explain the similarity in their gross behavioral phenotypes. 1. Pflugrad et al. (1997) Development 124:1699-1709. 2. Hall, German and Miller (1997) 11th Annual C. elegans meeting. 3. J.G. White et al. (1986) Phil. Trans. R. Soc. Lond 314:1-340. 4. J.G. White et al. (1992) Nature 355:838-41.

Coulson AR et al. (1989) Worm Breeder's Gazette "genome map."

Ameer H, Albertson DG, Sulston JE, Coulson AR, Waterston RH, Fishpool RM

[Worm Breeder's Gazette, 1989]

The map is now widely distributed electronically (see WBG 10(3), 67), but we are once again providing a summary for the gazette in the form of an output from the routine CHPLT. Do note that this is a provisional best guess, and that some linkages may later go away: please enquire if you need to know about the status of particular areas. When you receive cosmid clones, as stabs, please IMMEDIATELY streak them out on selective medium, pick small colonies, and grow 4ml minipreps (protocol from Alan Coulson if needed). For some cosmids, larger preps are liable to yield deleted DNA. Check that cosmid DNA appears full size (runs slower than lambda on agarose gels), then freeze a sample of good cells in 20% glycerol at -70 C. MRC computer account 'ARC' does not exist; Alan and John share account JES. A database node is now open at Seattle: modem number 206-467-2957; operator Phil Meneely. The summary of clone types given on the next page may be helpful when you are deciding which clones to request for your research. To reveal the most suitable clones for microinjection, the buried clones need to be displayed by the routine CONTASS; we will help you to do this if you ask. [See Figures 1- 3]

Yuan JY et al. (1987) Worm Breeder's Gazette "Tc4, a new C elegans transposon."

Horvitz HR, Finney M, Yuan JY

[Worm Breeder's Gazette, 1987]

Mutator strains isolated on the basis of increased Tc1 transposition in Phil Anderson's laboratory have provided a powerful tool to use in the molecular cloning of C. elegans genes. One can look for mutator- induced alleles of a gene of interest and then use Tc1 as a probe to determine whether Tc1 has inserted into the gene. One difficulty in using this approach has been that not all mutator-induced mutations are caused by insertion of Tc1. We have discovered that two mutator- induced unc-86 alleles, u371 (isolated by Marty Chalfie) and n1351 ( isolated by Stuart Kim), contain two different kinds of non-Tc1 insertions. With the hope of identifying more worm transposons, we have cloned both of these insertions. The insertion in u371 was found to be the same as an insertion isolated in Phil Anderson's laboratory; this insertion is now called Tc3. The 1.8 kb insertion in n1351, now called Tc4, was found to have also inserted into ced-4 (see abstract by Junying Yuan and Bob Horvitz in this WBG). Southern blot analyses showed that there are about 20 copies of Tc4 in both the Bristol and Bergerac strains, with a few polymorphisms between these strains. Although we have not examined our parental mutator strains for the number of Tc4 copies, one 10x-backcrossed mutant generated from mut-2 contains a few extra bands of Tc4, consistent with the hypothesis that Tc4 is activated in mut-2. Tc4 has a number of properties that indicate that it is a foldback element, i.e. it consists of a pair of inverted repeat DNA sequences. First, restriction enzyme mapping showed that Tc4 has symmetrical restriction sites. Second, it inverts its position in a plasmid vector very frequently when it is carried in a RecA strain. Third, presumably due to its foldback structure, Tc4 is difficult to label using the standard oligo-labelling method unless the element is first cut in the middle by a restriction enzyme. Northern blot analyses have shown that N2 expresses at least four poly-A(+) RNAs that can hybridize to Tc4. One is about 5 kb, one is about 3 kb and two are about 1.7 kb. The size differences could be due to heterogeneity in the size and structure of Tc4 elements because on Southern blots the intensity of different Tc4 bands are very different. We are interested in seeing if extra classes of Tc4 transcripts are present in the mutator strains, and if so whether such transcripts can account for the mutator activity.