C. elegans detects chemicals with 11 pairs of bilaterally symmetric sensory neurons. All of the right-left members of these pairs share similarity in lineage, morphology, and synaptic connectivity. However, one of these pairs (ASE) expresses genes asymmetrically1. ASEL expresses two putative chemoreceptor guanylyl cyclases
gcy-6&7 and the homeobox gene
lim-6, while ASER expresses a different guanylyl cyclase
gcy-5. The ASE neurons are important for chemotaxis to soluble attractants including salts3. We tested whether the asymmetry in expression pattern correlated with an asymmetry in function by ablating ASER, ASEL, or both neurons in individual worms and tracked each animal during chemotaxis in gradients of ammonium chloride, sodium acetate, potassium acetate, and ammonium acetate. To measure chance performance, we tracked worms (n=74) in the absence of a gradient, but analyzed them as if they were in a gradient. Most ASER- (n=29) and ASE- (n=27) worms failed to reach the peak of the NH4Cl gradient, while most ASEL- worms (n=22) reached the peak similar to sham worms (anaesthetized and recovered but not ablated; n=35). Likewise, most ASER- (n=17) and ASE- (n=15) worms failed to reach the peak of the K-acetate gradient, while most ASEL- worms (n=20) reached the peak similar to sham worms. Surprisingly, most ASEL- (n=26) and ASE- (n=12) worms failed to reach the peak of the Na-acetate gradient, while most ASER- worms (n=25) reached the peak similar to sham worms. Worms did not perform better than chance in the ammonium-acetate gradient (n=37). Thus, ASER controls chemotaxis to Cl- and K+, while ASEL controls chemotaxis to Na+. In
lim-6 deletion mutants
gcy-5 is ectopically expressed in ASEL, while
gcy-6&7 expression is correctly restricted to ASEL2. To examine if LIM-6 specifies asymmetry in ASE function, we tested whether ASE neurons retain their asymmetric function in
lim-6 mutants. In contrast to wildtype worms, many ASER-
lim-6 worms (n=28) were able to reach the peak of the ammonium chloride gradient. Thus, a homeobox gene is involved in breaking symmetry in neuronal function. 1. Yu et al (1997) PNAS 95:3384-7 2. Hobert et al (1999) Dev 126:1547-62 3. Bargmann & Horvitz (1991) Neuron 7:729-42