We have characterized an EMS derived mutant strain,
lrn-2, which shows deficits in both sensory integration and a wide variety of associative learning paradigms. Our experiments suggest that while sensory integration and associative learning mechanisms share genes in common, they act within independent pathways.Snip-SNP mapping and genome sequencing suggested that the locus of the
lrn-2 mutation was the gene
scd-2, which is homologous to human anaplastic lymphoma kinase. This was supported by
lrn-2 and
scd-2 failing to complement each other after a cross, and by a wild type
scd-2 containing fosmid successfully rescuing associative learning in a
lrn-2 background.The test of associative learning used in this project involved learning about pathogenic bacteria. The N2 control strain learns to associate the pathogenicity of PA14, a strain of P. aeruginosa, with the odor of the bacteria after 4 hour exposure. This results in N2 worms leaving the PA14, and migrating to a safe E. coli lawn on the other side of the plate. The
lrn-2 mutants do not learn this association and remain on the pathogenic bacteria. The sensory integration deficit is demonstrated by the mutant's inability to integrate two cues by crossing an aversive copper barrier to reach an attractive diacetyl odorant.Both learning and sensory integration involve processing of multiple sensory cues leading to altered behavioral output. While sensory integration does not require these changes to persist, learned behaviors do, as memories.
lrn-2/scd-2 plays a role in both sensory integration and associative learning; however, we have found that each of these psychological processes require
lrn-2/scd-2 expression in different cells. Furthermore, the gene
fsn-1 has been shown to have an upstream suppressive effect on
scd-2 sensory integration, but we have found that in an associative learning assay,
fsn-1 may act differently, downstream of
scd-2. While a worm must integrate presented sensory cues, the process of associating these cues and remembering this association for later recall requires a different mechanism then the immediate response to integration of cues. Further investigation will involve identifying the site of
lrn-2/scd-2 activity in associative learning, identifying its place within the associative learning molecular pathway, and using pharmaceutical antagonists to disrupt
scd-2 activity to identify its specific role in learning.