Ling, Linsay, Mendoza, Steve, Sherry, Tim, Nowak, Nathaniel, Arisaka, Katsushi, Jiang, Karen, Haller, Leonard
[
International Worm Meeting,
2015]
Perception and navigation through space require accurate translation and transmission of sensory input to motor output. On a linear temperature gradient, Caenorhabditis elegans demonstrate a distinct behavioral phenotype in which they frequently travel along isotherms, maintaining sensitivity within 0.05 degC. This isothermal attractor state is correlated with movement at a constant and maximal velocity. We investigate how AIY, a first layer interneuron and postsynaptic partner to AFD thermosensory neuron, is able to integrate thermal information to return specific well-defined behavioral phenotypes. Prior observations of neural activity in vivo involve partial paralysis or constraint of the worm while stimuli is applied. Other systems circumvent this limitation by re-centering the stage; this generates an external force during stage acceleration introducing another stimulus. We overcome these two primary obstacles through the implementation of a novel automated worm-tracking epi-fluorescent microscope. The three-camera microscope system mounted on a movable XY stage captures dynamic Ca+2 signals in Cameleon-labeled neurons while the nematode navigates unconstrained along the temperature gradient. Implementing this set up, we observed that the greatest temperature difference occurs between the extremes of the head movement while along isotherms which phase lock with fluorescence response in AIY. The steady Ca+2 waveform in AIY suppresses reversals and maintains high speeds to downstream motor circuitry. .
Atamdede, Sean, Haller, Leonard, Kao, Michelle, Mendoza, Steve, Madruga, Blake, Agarwal, Neha, Nowak, Nathaniel, Sunyoto, Amanda, Sherry, Tim, Jiang, Karen, Cheng, Shirley, Vanmali, Bobby, Trusz, Guillaume, Arisaka, Katsushi, Pellionisz, Peter, Woolfork, De'Marcu, Sagadevan, Addelyn, Kim, Taejoon, Ling, Linsay, Lam, Brian
[
International Worm Meeting,
2015]
For students, the study of model organisms presents an opportunity to learn various general science and research disciplines; however, each model organism has it's own set of advantages. Chiefly, Caenorhabditis elegans are excellent model organisms to study neuroscience and biophysics due to its availability, tractability, relatively simple nervous system, and it's patently observable behavior. Here in the Elegant Mind Club at UCLA, we provide undergraduate students a unique hands-on experience working with C. elegans and a chance to present their own scientific methods of interest, allowing them to explore the nature of scientific research and understand the conclusions drawn from their data. In our laboratory, undergraduate students are entirely responsible for maintaining and culturing the worms as well as building and refining their experimental systems. Direct involvement with the biological samples teaches students the discipline of working with chemicals and maintaining sterility. Published papers and online resources such as WormBook, WormAtlas, and Caenorhabditis Genetics Center provide students with a source of well-established methods and techniques to serve as a basis for their own studies. Manual practice in hardware development permits students to personally hone their experiment to be the most controlled and reproducible systems. As of now, systems for thermotaxis, electrotaxis, chemotaxis, phototaxis, durotaxis, as well as behavior within a magnetic field and the absence of stimuli have been reproduced and improved by our members. Our laboratory begun with a few core members and have expanded to accommodate more than 80 students from different universities over the world and we hope to encourage more students to approach scientific research with enthusiasm.
[
1987]
The concept of developmentally programmed senescence has been outlined by Leonard Hayflick (this volume), and examples from development have been used as exemplars of "developmentally programmed senescence" (Richard Russell, this volume). Unlike development, senescence has probably evolved in the absence of direct selection for increased longevity, perhaps as a direct result of the absence of such selection. (For an excellent review see Charlesworth.) A popular evolutionary model that has received experimental support suggests that senescence may result from pleiotropic effects of selection for adaptive life history characteristics. In the literature on aging, less rigorous arguements have been used to suggest that in human evolution, a delay in the age of senescence has been indirectly selected for by means of so-called longevity assurance or longevity-determinant genes. However, all explanations for the evolution of senescence are theoretical, and, with few exceptions, remain largely untested. Like Dr. Hayflick and Russell, I will assume that by developmental programming we mean genetic specification. I will use a general definition so as not to preclude examples that fail to meet one or more of the rigid criteria defined by Russell (this volume). This less rigid definition of programmed aging is necessary, because unlike development, where genetics has been successfully applied for 50 years, examples of genetic specification of senescent processes are quite few. In the literature on aging, it is still not widely accepted that mutants can alter fundamental patterns of senescent events in well-defined ways. One purpose of this presentation is to outline a few examples. In senescence, large batteries of new genes are not differentially regulated; this is quite unlike development, where many genes are differentially regulated. The molecular etiology of senescence is unknown in almost every instance and, as such, makes the study of aging a fascinating area for inquiry. If senescence is unlike development in lacking differential gene regulation, what are the approaches that are likely to yield useful results in the analysis of senescence and the aging process? The developmental genetic paradigm is a useful, indeed essential, theoretical construct for approaching the aging process in an experimental context. The lack of a suitable model organism in which classical and molecular genetics can be productively combined with other experimental techniques has impeded our understanding of senescence. Despite a general lack of evidence for genetic specification, there are instances where genetic specification is clearly evident; the analysis of mutational events that alter normal senescence in well-defined ways demonstrates this point. These instances also provide experimental models for dissecting the aging