Walker MY et al. (2000) Chromosoma "Hanging on to your homolog: the roles of pairing, synapsis and recombination in the maintenance of homolog adhesion."

Walker MY, Hawley RS

[Chromosoma, 2000]

Homologous chromosomes initially undergo weak alignments that bring homologous sequences into register during meiosis. These alignments can be facilitated by two types of mechanisms: interstitial homology searches and telomere-telomere alignments. As prophase (and chromatin compaction) proceeds, these initial pairings or alignments need to be stabilized. In at least some organisms, such as Saccharomyces cerevisiae and S. pombe, these pairings can apparently be maintained by the creation of recombination intermediates. In contrast, synapsis during zygotene may be able to facilitate and/or maintain chromosome pairing even in the absence of exchange in several higher organisms. It thus seems possible that the synaptonemal complex plays a role both in maintaining homolog adhesion during meiotic prophase and, more speculatively, in facilitating meiotic exchange.

Rankin CH J Neurogenet "But can they learn? My accidental discovery of learning and memory in C. elegans."

Rankin CH

[J Neurogenet]

I did not set out to study <i>C. elegans</i>. My undergraduate and graduate training was in Psychology. My postdoctoral work involved studying learning and memory in 1mm diameter juvenile <i>Aplysia californica</i>. As a starting Assistant Professor when I attempted to continue my studies on Aplysia I encountered barriers to carrying out that work; at about the same time I was introduced to <i>Caenorhabditis elegans</i> and decided to investigate whether they could learn and remember. My laboratory was the first to demonstrate conclusively that <i>C. elegans</i> could learn and in the years since then my lab and many others have demonstrated that <i>C. elegans</i> is capable of a variety of forms of learning and memory.

White JG (2000) Int J Dev Biol "Worm tales."

White JG

[Int J Dev Biol, 2000]

1969 was a landmark year. But for me it was not Neil Armstrong's giant leap or Woodstock heralding the beginning of the end of the sixties that sticks in my mind. It was a visit I made to Cambridge to meet a "bloke who is starting a new project to study some sort of worm", as my head of department at the Medical Research Council's National Institute of Medical Research informed me...

Ausubel FM (2018) Annu Rev Genet "Tracing My Roots: How I Became a Plant Biologist."

Ausubel FM

[Annu Rev Genet, 2018]

My trajectory to becoming a plant biologist was shaped by a complex mix of scientific, political, sociological, and personal factors. I was trained as a microbiologist and molecular biologist in the late 1960s and early 1970s, a time of political upheaval surrounding the Vietnam War. My political activism taught me to be wary of the potential misuses of scientific knowledge and to promote the positive applications of science for the benefit of society. I chose agricultural science for my postdoctoral work. Because I was not trained as a plant biologist, I devised a postdoctoral project that took advantage of my microbiological training, and I explored using genetic technologies to transfer the ability to fix nitrogen from prokaryotic nitrogen-fixing species to the model plant Arabidopsis thaliana with the ultimate goal of engineering crop plants. The invention of recombinant DNA technology greatly facilitated the cloning and manipulation of bacterial nitrogen-fixation (nif) genes, but it also forced me to consider how much genetic engineering of organisms, including human beings, is acceptable. My laboratory has additionally studied host-pathogen interactions using Arabidopsis and the nematode Caenorhabditis elegans as model hosts. Expected final online publication date for the Annual Review of Genetics Volume 52 is November 23, 2018. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

Horvitz HR (2003) Chembiochem "Worms, life, and death (Nobel lecture)."

Horvitz HR

[Chembiochem, 2003]

I never expected to spend most of my life studying worms. However, when the time came for me to choose an area for my postdoctoral research, I was intrigued both with the problems of neurobiology and with the approaches of genetics. Having heard that a new "genetic organism" with a remarkably simple nervous system was being explored by Sydney Brenner - the microscopic soil nematode Caenorhabditis elegans - I decided to join Sydney in his efforts.

Schaffner KF (1998) Philosophy of Science "Model organisms and behavioral genetics - A rejoinder."

Schaffner KF

[Philosophy of Science, 1998]

In this rejoinder to the three preceding comments, I provide some additional philosophical warrant for the biomedical sciences' focus on model organisms. I then relate the inquiries on model systems to the concept of 'deep homology', and indicate that the issues that appear to divide my commentators and myself are in part empirical ones. I cite recent work on model organisms, and especially C. elegans that supports my views. Finally, I briefly readdress some of the issues raised by Developmental Systems Theory.

Vanfleteren JR et al. (1994) Mol Phylogenet Evol "Molecular genealogy of some nematode taxa as based on cytochrome c and globin amino acid sequences."

Moens L, Vanfleteren JR, Trotman CNA, Tweedie SA, Van de Peer Y, Lu L, Van Hauwaert ML, Blaxter ML

[Mol Phylogenet Evol, 1994]

We have begun to reconstruct the ancient history of the nematode phylum based on cytochrome c and globin amino acid sequences. The data suggest that the nematode ancestor diverged from a line leading to mammals about 1 billion years ago and that the most recent common ancestor of the extant species Caenorhabditis elegans, Trichostrongylus colubriformis, Nippostrongylus brasiliensis, Ascaris suum, and Pseudoterranova decipiens lived about 550 MY ago. The rhabditids and strongylids emerged as one offshoot of this ancestor, the ascarids as another. Rhabditids and strongylids diverged some 400 MY ago, whereas the genera Trichostrongylus and Nippostrongylus diverged slightly over 200 MY ago. A gene duplication event in the strongylid branch is predicted to have occurred around 250-335 MY ago. There are two globin genes in Nippostrongylus, expressed in anatomically distinct compartments (body and cuticle), and the single sequence from Trichostrongylus is most like the Nippostrongylus body globin gene. A strikingly different duplication event occurred within the same period in the line leading to the extant ascarid genera, creating a single polypeptide containing two globin domains. The genera Ascaris and Pseudoterranova diverged some 150-250 MY ago. Interestingly, the second globin repeat evolved at a faster rate in both species examined. This is possibly related to the acquisition of an unusual carboxyterminal extension, composed of alternating positively and negatively charged residues, that is necessary for the assembly of several monomers into the native polymeric molecules.

Roxani Gatsi et al. (2005) International Worm Meeting "Suppressor screens for the dissection of the IP3 signalling pathway in the pharynx"

Roxani Gatsi, Howard Baylis

[International Worm Meeting, 2005]

IP3 mediated calcium signalling in C. elegans determines specificity of cellular responses to extracellular stimuli. Specialized IP3 receptors (IP3Rs), which are located on the endoplasmic reticulum membrane, regulate cytoplasmic calcium concentrations that determine various cellular functions. One of these functions is the up-regulation of pharyngeal pumping in response to food (Walker et al, 2002a). Relatively little is known about the IP3-mediated regulation of the rhythmic pumping of the pharynx. Walter et al (2002b) has shown that interaction between IP3Rs and myosin are required for regulation of pharynx pumping but not for other physiological rythmic functions in C. elegans, indicating the importance of protein interactions for determining specificity. In order to identify additional components of the IP3 signalling pathway in the pharynx we performed genetic suppressor screens using an IP3R mutant (sa73), which shows reduced pharyngeal pumping. We have isolated various mutants that suppress various defects of the sa73 phenotype. The results from the characterization of these mutants, as well as the approach to map the mutations will be presented. Walker DS., et al. (2002a) Mol Biol Cell 13, 1329-1337. Walker DS., et al. (2002b) Curr Biol 12, 951-956

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.

Birgitta Olofsson (2009) European Worm Neurobiology Meeting "Optimal foraging in C.elegans"

Birgitta Olofsson

[European Worm Neurobiology Meeting, 2009]

Variation in food quality and abundance requires animals to choose whether to stay on poor food patch or wander off in search of better food. Although optimal foraging choice is central to evolutionary survival, the molecular and neuronal mechanisms underlying it are poorly understood. I will present my work on this problem in C.elegans.