Predators and prey co-evolve, each maximizing their own fitness, but the effects of predator–prey interactions on cellular and molecular machinery are poorly understood. Here, we study this process using the predator Caenorhabditis elegans and the bacterial prey Streptomyces, which have evolved a powerful defense: the production of nematicides. We demonstrate that upon exposure to Streptomyces at their head or tail, nematodes display an escape response that is mediated by bacterially produced cues. Avoidance requires a predicted G-protein-coupled receptor, SRB-6, which is expressed in five types of amphid and phasmid chemosensory neurons. We establish that species of Streptomyces secrete dodecanoic acid, which is sensed by SRB-6. This behavioral adaptation represents an important strategy for the nematode, which utilizes specialized sensory organs and a chemoreceptor that is tuned to recognize the bacteria. These findings provide a window into the molecules and organs used in the coevolutionary arms race between predator and potential prey.

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The organization of neurons and the maintenance of that arrangement are critical to brain function. Failure of these processes in humans can lead to severe birth defects, mental retardation, and epilepsy. Several kinesins have been shown to play important roles in cell migration in vertebrate systems, but few upstream and downstream pathway members have been identified. Here, we utilize the genetic model organism Caenorhabditis elegans to elucidate the pathway by which the C. elegans Kinesin-1 Heavy Chain (KHC)/KIF5 ortholog UNC-116 functions to maintain neuronal cell body position in the PHB sensory neurons. We find that UNC-116/KHC acts in part with the cell and axon migration molecules UNC-6/Netrin and UNC-40/DCC in this process, but in parallel to SAX-3/Robo. We have also identified several potential adaptor, cargo, and regulatory proteins that may provide insight into the mechanism of UNC-116/KHC's function in this process. These include the cargo receptor UNC-33/CRMP2, the cargo adaptor protein UNC-76/FEZ and its regulator UNC-51/ULK, the cargo molecule UNC-69/SCOCO, and the actin regulators UNC-44/Ankyrin and UNC-34/Enabled. These genes also act in cell migration and axon outgrowth; however, many proteins that function in these processes do not affect PHB position. Our findings suggest an active posterior cell migration mediated by UNC-116/KHC occurs throughout development to maintain proper PHB cell body position and define a new pathway that mediates maintenance of neuronal cell body position. IN the developing nervous system, neurons must migrate to their proper position and then maintain that position throughout the life of the animal. This is an important process, as aberrant neuronal position is thought to cause severe birth defects such as lissencephaly (fewer gyri), pachygyria (fat gyri), and various heterotopias (mislocalization of brain matter). These defects can lead to severe mental retardation and epilepsy in humans (Verrotti et al. 2010;Liu 2011).In vertebrates, several different kinesins are necessary for proper cell migration (Zhang et al. 2009;Tsai et al. 2010;Vidal et al. 2012). For example in mice, KIF5C/Kinesin-1 Heavy Chain (KHC) is necessary for the migration of neurons into the cerebral cortex (Vidal et al. 2012). In rats, at least one isoform of the heavy chains of Kinesin-1, -2, -3, -8, and -11 mediates cell migration to the intermediate zone and cortical plate (Tsai et al. 2010). However, the mechanism by which kinesins affect cell migration is still poorly understood.During cell migration, neurons are directed by an array of highly conserved guidance cues (Hatten 2002;Rorth 2009). In vertebrates and invertebrates, the secreted ligand UNC-6/ Netrin and its receptors UNC-40/DCC and UNC-5/Unc5, as well as the secreted ligand SLT-1/Slit and its receptor SAX-3/Robo, are necessary for positioning along the dorsalventral axis (Hedgecock et al. 1990;Ishii et al. 1992;Leung-Hagesteijn et al. 1992;Hamelin et al. 1993;Chan et al. 1996;Kim et al. 1999;Bradford et al. 2009). Wnts, b...

Predators and prey co-evolve, each maximizing their own fitness, but the effects of predator-prey interactions on cellular and molecular machinery are poorly understood. Here, we study this process using the predator Caenorhabditis elegans and the bacterial prey Streptomyces, which have evolved a powerful defense: the production of nematicides. We demonstrate that upon exposure to Streptomyces at their head or tail, nematodes display an escape response that is mediated by bacterially produced cues. Avoidance requires a predicted G-protein-coupled receptor, SRB-6, which is expressed in five types of amphid and phasmid chemosensory neurons. We establish that species of Streptomyces secrete dodecanoic acid, which is sensed by SRB-6. This behavioral adaptation represents an important strategy for the nematode, which utilizes specialized sensory organs and a chemoreceptor that is tuned to recognize the bacteria. These findings provide a window into the molecules and organs used in the coevolutionary arms race between predator and potential prey.