[
International Worm Meeting,
2005]
The behavioural avoidance of pathogens minimizes both the inflicted damage and the costs imposed by mounting an immune response required for fighting an infection. Such a strategy should be highly economic and widespread among animals, yet only little is currently known about its occurrence and the underlying mechanisms. In this study, we explore the genetics of pathogen avoidance behaviour in C. elegans. We show that two distinct behavioural defences are mediated through the insulin-like receptor pathway. Since this pathway also contributes to immunity, our study provides the first evidence for a genetic link between physiological and behavioural defences. Our results highlight the importance of insulin signalling as a major life history switch, which determines the optimal life history strategy in response to environmental cues.
[
FASEB J,
2007]
Pathogens cause damage, and their elimination requires activation of the costly immune response. A highly economic defense strategy should thus be the behavioral avoidance of pathogens, as manifested in humans by all aspects of hygiene or revulsion at pathogen-rich material. Despite its potential importance, behavioral defenses have as yet received only little attention in biomedical research--in stark contrast to the physiological immune system. In the present study, the genetics of such behavioral defenses are elucidated in a simple model organism, the nematode Caenorhabditis elegans. We show for the first time that mutations in the insulin-like receptor (ILR) pathway lead to two distinct behavioral responses against pathogenic strains of the Gram-positive bacterium Bacillus thuringiensis (BT), including the physical evasion of pathogens and their reduced oral uptake. Since this pathway also contributes to nematode stress resistance, the results surprisingly reveal a genetic link between physiological and behavioral defenses. Considering that many signaling pathways have conserved their functions across evolution, including the ILR pathway, this signaling cascade may represent an interesting candidate regulator for behavioral defenses in more complex organisms, including humans.--Hasshoff M., Bohnisch C., Tonn D., Hasert B., Schulenburg H. The role of Caenorhabditis elegans insulin-like signaling in the behavioral avoidance of pathogenic Bacillus thuringiensis.
[
International Worm Meeting,
2009]
Aging is a complex physiological process and numerous aging theories have been proposed. One of the leading models is the free radical theory of aging, which suggests that the accumulation of reactive oxygen species (ROS), like superoxide (O2-) and hydrogen peroxide (H2O2), causes protein, lipid and DNA damage and leads to the observed age-related decline of cells and tissues. To directly monitor the onset and extent of oxidative stress during the lifespan of C. elegans, we utilize two complementary approaches. In the first approach, we use the fluorescent H2O2-sensor protein HyPer (Belousov, 2006) to evaluate the accumulation of endogenous H2O2 in the muscle cells of C. elegans. This ratiometric sensor protein has two excitation maxima, which substantially change in the presence of H2O2. With this tool, we are now able to determine and monitor endogenous H2O2 levels over the whole life span of a worm population. In the second approach, we use a highly quantitative mass spectrometry based thiol trapping technique termed OxICAT to identify the protein targets of oxidative stress in aging animals. This technique allows us not only to detect and quantify oxidative thiol modifications in hundreds of different proteins in a single experiment but enables us to identify the affected proteins and to define their redox-sensitive cysteine(s). Using this technique we were able to determine the redox status of numerous C. elegans proteins and monitor their age-related changes. The combination of these techniques provides us now with valuable insights into the underlying mechanism of aging and into the role that oxidative stress plays in this process. Reference: Belousov, V.V., et al., Nat Methods, 2006. 3(4). Maike Thamsen and Daniela Knoefler contributed equally to the work for this abstract.
Berriman, Matt, Howe, Kevin, Kersey, Paul, Stein, Lincoln, Harris, Todd, Sternberg, Paul, Schedl, Tim
[
International Worm Meeting,
2015]
WormBase has existed for 15 years and has evolved in many ways. The new website is fully operational and has made the process of adding new data types, displays, and tools easier. Behind the scenes we are piloting an overhaul of the underlying database infrastructure to allow us to handle the ever increasing data, have the website perform faster, and allow more frequent updates of information. This is a critical time for the project, as we face considerable pressure from two directions. The first is that our funders really want us to do more with less. We are responding to this by leading the way in making curation (the process of extracting information from papers and data sets into computable form) more efficient using a new version of Textpresso (to be released later this calendar year); by discussing with other model organism information resources ways to work together to be more efficient and inter-connected; and by seeking additional sources of funding. The second, delightful, pressure is an increase in data and results generated by the C. elegans and nematode communities. While we are handling this increase by changes in our software for curation, the database infrastructure, and the website, we do need your help. Many of you have helped us over the last few years to identify data in your papers or by sending us data directly. We now need you to help with a few types of information by submitting the data via specially designed, user-friendly forms that ensure good quality and the use of standard terminology. In particular, we have a large backlog of uncurated information associating alleles with phenotypes. We pledge to make this process as painless as possible, and to improve WormBase's description of phenotypes with your feedback, starting at this meeting at the WormBase booth, workshops and posters. With your help, continual improvement of our efficiency, and additional sources of funding, we are optimistic that we can do much more with even somewhat less effort.Consortium: Paul Davis, Michael Paulini, Gary Williams, Bruce Bolt, Thomas Down, Jane Lomax, Todd Harris, Sibyl Gao, Scott Cain, Xiaodong Wang, Karen Yook, Juancarlos Chan, Wen Chen, Chris Grove, Mary Ann Tuli, Kimberly Van Auken, D. Wang, Ranjana Kishore, Raymond Lee, John DeModena, James Done, Yuling Li, H.-M. Mueller, Cecilia Nakamura, Daniela Raciti, Gary Schindelman.