Abstract:
The study of sensory systems in humans is a vital area of study to further pursue our knowledge of the mechanisms occurring in the nervous systems. However due to the complications surrounding human testing, model organisms such as C. elegans worms can be utilized as a comparison to create paradigms relevant to human sensory systems as the genetic basis for both organisms is related amongst other factors such as the worm’s rapid reproductive cycle. Using RNAi treatment on C. elegans we tested the effects of inhibiting the synthesis of particular proteins in relation to the organism’s ability to detect and consequently move towards – that is chemosensation and chemotaxis - characteristically favorable odorants. This type of work hopes to build a basis for understanding the network of chemosensory signaling systems in humans and the corresponding proteins produced by particular gene sequences. Results suggested that gene sequence Srb-16 was not involved in encoding for a protein involved in chemosensation although contrary to previous experiments. The second gene sequence that was analyzed, F35B1.3- a mostly unknown sequence- was shown to likely encode for a protein in the sensory olfactory system as characteristic chemosensation behavior of C. elegans was altered.
Introduction:
This experiment was carried out to test the role of gene sequences Srb-16 and F34B1.3 in the chemosensation of C. elegans. Using RNAi treatment, the genes were inhibited from encoding their specific proteins and the resulting effect was analyzed to determine whether or not the genes play a role in chemotaxis of diacetyl. Diacetyl (DA) is a toxic buttery smelling odorant normally attractive to C. elegans. By observing the worms post RNAi treatment in their ability to detect and move towards DA, conclusions were drawn as to whether the gene sequence