McGill, C.J. et al. (2017) International Worm Meeting "Comparing miRNAs across developmental stages of C. elegans and other nematodes."

Macchietto, M., Phan, J.L., McGill, C.J., Serra, L., Mortazavi, A., Rodriguez, B.

[International Worm Meeting, 2017]

MicroRNAs(miRNAs) are small,17-22bp, non-coding RNAs that have been shown to have a significant regulatory effect on gene expression. Measuring this regulation is vital to understanding how gene expression progresses through developmental programs. We are interested in studying this through the Caenorhabditis elegans developmental model system. Due to older technologies, previous studies had to be done on thousands of worms at a time, and thus, the resolution was poor. New technology has enabled us to cut that number to few worms, which has drastically improved the resolution. We, also, will be profiling miRNAs at every stage of development to study the progression of miRNAs. We will compare our results to other nematodes such as Steinernema carpocapsae and Caenorhabditi angaria. This will be the first comparison of miRNAs expression at the single-worm level among distant nematode species with a focus on miRNAs involved in gene regulation during development.

McGill, C.J. et al. (2019) International Worm Meeting "Variations in microRNA expression during development of divergent Caenorhabditis elegans strains."

Mortazavi, A., Serra, L., Rodriguez, I.M, McGill, C.J.

[International Worm Meeting, 2019]

MicroRNAs(miRNAs) are small, 17-22nt, non-coding RNAs that play a critical role in post-transcriptional regulation including during development. We are interested in studying the impact of microRNA expression variation in Caenorhabditis elegans strains by characterizing the expression of miRNAs and mRNA at the L1 stage using twelve Caenorhabditis elegans Natural Diversity Resource (CeNDR) strains that constitute the "divergent set". Our goal is to investigate variations in miRNA and mRNA profiles at the L1 stage in response to developmental stress. Preliminary results indicate that each strain has a distinct gene expression profile. We also found that N2 expresses more dauer related genes compared to CB4856. We will compare eleven CeNDR strains to N2 and identify key differences in miRNAs and mRNA expression.

Barnes TM (1994) Worm Breeder's Gazette "The Structure of the C. elegans Genome and Implications For Function"

Barnes TM

[Worm Breeder's Gazette, 1994]

The Structure of the C. elegans Genome and Implications for Function. Tom Barnes, Department of Biology, McGill University, Montreal, PQ H3A lBl Canada

Barnes TM (1994) Worm Breeder's Gazette "Genome Parametrics, or Look, I Can Use Query and Tablemaker!"

Barnes TM

[Worm Breeder's Gazette, 1994]

Genome Parametrics, or Look, I can use Query and Tablemaker! Tom Barnes Deptartment of Biology, McGill University, Montreal PQ H3AlB1 Canad

Denham DA et al. (1989) J Helminthol "Experimental Brugia pahangi and B. malayi infections of callitrichid primates."

Suswillo RR, Hetherington CM, Denham DA

[J Helminthol, 1989]

The callitrichid primates, Callithrix jacchus jacchus (the marmoset) and Saguinus labiatus (the tamarin) were inoculated with infective larvae of Brugia malayi and B. pahangi. Microfilaraemia at low levels developed in 3 out of 4 C.j. jacchus infected with B. malayi and living or dead adult worms found in all 4. Only one of 4 C.j. jacchus became microfilaraemic (mf + ve) when given B. pahangi and adults were found in two. Of 4 S. labiatus given B. pahangi one became very lightly mf + ve and adults were found in 3. It is concluded that these animals are not suitable hosts for chemotherapeutic experiments.

Pennisi E (1996) Science "Worm genes imply a master clock."

Pennisi E

[Science, 1996]

What 's the secret to long life? For the nematode Caenorhabditis elegans, it's slow, easy living, in which all life's events occur in a leisurely rhythm, according to work described on page 1010 of this issue. The new research, by Siegfried Hekimi and Bernard Lakowski of McGill University in Montreal, identifies four genes that, when mutated, can make these worms use energy more efficiently, feed and swim at a slower pace-and live many times their normal life-span. Some of the experimental nematodes lived for almost 2 months, far longer than their expected 9 days.

Kravtsov, V. et al. (2013) International Worm Meeting "The effects of aging on dendritic plasticity and PVD-FLP branch coexistence."

Podbilewicz, B., Oren-Suissa, M., Kravtsov, V.

[International Worm Meeting, 2013]

Self-avoidance, tiling and coexistence are the main mechanisms that enable the best dendritic coverage. C. elegans undergoes aging-associated changes that ultimately lead to decreased functionality of the organism, including its neurological functions. Recent research has shown that the nervous system of C. elegans undergoes changes and alterations during aging including dendritic morphology (Tank et al., 2011). We study dendritic plasticity, aging and spatial dendritic organization of two highly arborized mechanoreceptors in C. elegans, PVD and FLP (Oren-Suissa et al., 2010). PVD dendrites of L4s and young adults show regenerative ability following dendrotomy (laser induced severing of dendrites). Our working hypothesis is that in older ages this ability to regenerate is compromised. Previous studies and our preliminary results indicate that PVD and FLP do not overlap in larval stages (Smith et al., 2010). In addition, dendrites within each bilateral PVD do not overlap through a self-avoidance mechanism (Smith et al., 2012). We found that (1) the coverage fields of the PVD and FLP overlap in adult worms, which indicates coexistence and not tiling. This overlap increases as the worm ages. (2) PVDs show aberrant arborization at the age of 9 days of adulthood. (3) Dramatic increase in self-avoidance defects as animals age. In humans many neurodegenerative diseases as well as generalized cognitive decline are associated with age, aberrant arborization or both (e.g. autism and Alzheimer's disease). However our understanding of how these disorders are triggered and aggravated is scarce. Our research provides an insight into the aging and regeneration process of individual neurons. Oren-Suissa, M., et al. (2010). Science 328, 1285-1288. Smith, C.J. et al. (2010). Developmental Biology 345, 18-33. Smith, C.J., et al. (2012). Nature Neuroscience 15, 731-737. Tank, E.M.H. et al. (2011). Journal of Neuroscience 31, 9279-9288.

Ewbank JJ et al. (1997) Science "Structural and functional conservation of the Caenorhabditis elegans timing gene clk-1."

Lussier M, Bussey H, Lakowski B, Ewbank JJ, Barnes TM, Hekimi S

[Science, 1997]

Mutations in the Caenorhabditis elegans gene clk-1 affect biological timing and extend longevity. The gene clk-1 was identified, and the cloned gene complemented the clk-1 phenotypes and restored normal longevity. The CLK-1 protein was found to be conserved among eukaryotes, including humans, and structurally similar to the yeast metabolic regulator Cat5p (also called Coq7p). These proteins contain a tandem duplication of a core 82-residue domain. clk-1 complemented the phenotype of cat5/coq7 null mutants, demonstrating that clk-1 and CAT5/COQ7 share biochemical function and that clk-1 acts at the level of cellular physiology.AD - Department of Biology, McGill University, 1205 Avenue Docteur Penfield, Montreal, Quebec, Canada H3A 1B1.FAU - Ewbank, J JAU - Ewbank JJFAU - Barnes, T MAU - Barnes TMFAU - Lakowski, BAU - Lakowski BFAU - Lussier, MAU - Lussier MFAU - Bussey, HAU - Bussey HFAU - Hekimi, SAU - Hekimi SLA - engSI - GENBANK/U81276SI - GENBANK/U81277PT - Journal ArticleCY - UNITED STATESTA - ScienceJID - 0404511RN - 0 (CAT5 protein)RN - 0 (CLK-1 protein)RN - 0 (Fungal Proteins)RN - 0 (Helminth Proteins)RN - 56-81-5 (Glycerol)SB - IM

McCormick, Allyson V. et al. (2009) International Worm Meeting "Characterization of seizure modifiers in worms lacking CaMKII function."

McCormick, Allyson V., Kraemer, Brian, Thomas, James H.

[International Worm Meeting, 2009]

Several C. elegans mutants have seizures with acute exposure to neurostimulants1,2 (e.g. pentylenetetrazole). Loss-of-function alleles of unc-43, the worm homologue of CaMKII, have robust full-body convulsions easily induced by elevated temperature and drug exposure. To further describe worm seizures genetically, we have conducted pilot EMS screens for suppressors and enhancers of unc-43 seizures. Thus far, we have isolated fourteen suppressors and enhancers. Since unc-43(lf) animals have a range of phenotypes caused by a lack of function in specific tissues, modifiers have been classified by changes in seizures and a variety of other behaviors (e.g. spontaneous reversal rate). Characterization of genetic lesions is currently underway. Though identification can be time consuming, a key advantage of forward genetic screens is to isolate single point mutations that create more subtle variations in gene function. This is exciting since so little is known about modifiers in human epilepsies. Such modifiers may contribute to drug resistance, seizure frequency and developmental timing. 1Williams, S.N. et al. (2004). Hum Mol Genet (13) 2043-59. 2Locke, C.J. et al. (2006). Brains Res (1120) 23-34. .

Hannak E et al. (2002) J Cell Biol "The kinetically dominant assembly pathway for centrosomal asters in Caenorhabditis elegans is gamma-tubulin dependent."

Habermann B, Hannak E, Kirkham M, Gonczy P, Oegema K, Hyman AA

[J Cell Biol, 2002]

gamma-Tubulin-containing complexes are thought to nucleate and anchor centrosomal microtubules (MTs). Surprisingly, a recent study (Strome, S., J. Powers, M. Dunn, K. Reese, C.J. Malone, J. White, G. Seydoux, and W. Saxton. Mol. Biol. Cell. 12:1751-1764) showed that centrosomal asters form in Caenorhabditis elegans embryos depleted of gamma-tubulin by RNA-mediated interference (RNAi). Here, we investigate the nucleation and organization of centrosomal MT asters in C. elegans embryos severely compromised for gamma-tubulin function. We characterize embryos depleted of approximately 98% centrosomal gamma-tubulin by RNAi, embryos expressing a mutant form of gamma-tubulin, and embryos depleted of a gamma-tubulin-associated protein, CeGrip-1. In all cases, centrosomal asters fail to form during interphase but assemble as embryos enter mitosis. The formation of these mitotic asters does not require ZYG-9, a centrosomal MT-associated protein, or cytoplasmic dynein, a minus end-directed motor that contributes to self-organization of mitotic asters in other organisms. By kinetically monitoring MT regrowth from cold-treated mitotic centrosomes in vivo, we show that centrosomal nucleating activity is severely compromised by gamma-tubulin depletion. Thus, although unknown mechanisms can support partial assembly of mitotic centrosomal asters, gamma-tubulin is the kinetically dominant centrosomal MT nucleator.