In this paper in volume 14, issue 15 of Current Biology (pp. 13741379), we reported experimentson animals derived from the strain RB629 and carrying a deletion in latrophilin, lat-1
). Our studies showed that animals derived from this strain were emodepside resistant,and we concluded that this was due to a putative loss of function in lat-1
signaling. Afterpublication of this work, David Bell reported to us his unpublished observations on RB629.He could not balance lat-1
), nor could he identify animals homozygous for the deletion.We performed further analysis of RB629 and confirmed that animals derived from this strainare emodepside resistant. However, we have also subsequently found that animals derivedfrom the RB629 strain can lose the ok379
deletion but remain emodepside resistant. Therefore,the resistance in this strain does not correlate with the lat-1
deletion, and our conclusionsin this regard are invalid. The other substantial findings of the paper, the observation ofemodepside resistance in animals treated with RNAi for lat-1
and in mutants for other synapticproteins, are not affected by this revision.