While the mechanism that breaks left-right (L-R) anatomical asymmetry (handedness) has been described in C. elegans, we have found that at least one additional mechanism must exist to establish other handedness cues that generates L-R differences in the deployment of alternative cell death pathways (see abstract from our lab by Choi et al.). To assess whether such a system might affect a behavior in the worm, we investigated whether male mating behavior exhibits L-R handedness. Upon recognizing a hermaphrodite, males initiate backward locomotion and continuously scan along the hermaphrodite''s body. When their tails reach either the head or tail of the hermaphrodite, males turn to maintain contact and then continue backward locomotion on the opposite side of the hermaphrodite. We found that this turning behavior shows a distinct right-handed bias: when individual males were allowed to mate with
lin-2(
e1309) vulvaless hermaphrodites, >70% of the turns when made over the hermaphrodites'' body (away from the agar surface) and >55% of turns when made under the hermaphrodites'' body (toward the agar surface) are right-handed. To determine whether this bias in turning direction correlated with L-R asymmetry in the male mating structure, which results from stochastic EGL-1-dependent loss of sensory rays (Choi et al. abstract), we examined the turning bias in
egl-1(
n1084n3082) mutants. We were surprised to find that, although wild-type males lack rays more frequently on the right, the right-hand turning bias is actually increased in the
egl-1 mutant, in which no rays are lost and therefore rays are always symmetrically arranged. Thus, the intrinsic turning bias is even more apparent in males with symmetric mating structures. To assess whether this L-R behavioral bias is dependent on anatomical handedness, we analyzed
gpa-16(
it143) mutants in which the L-R asymmetry of the internal organs is reversed as a result of the reversal in the early embryonic symmetry break. Males with reversed anatomical asymmetry showed a virtually identical right hand bias in turning, demonstrating that a handedness-determining system that is independent of the previously described L-R symmetry breaking event must control this behavior. These findings raise the possibility that, analogous to brain laterality in humans, functionally L-R asymmetry in the C. elegans motor nervous system may be independent of anatomical handedness.