Willson, J., Amliwala, K., Davis, A., Cook, A., Cuttle, M.F., Kriek, N., Hopper, N.A., Connor, V., Harder, A., Walker, R.J. and Holden-Dye, L.
Latrotoxin receptor signaling engages the UNC-13-dependent vesicle-priming pathway in C. elegans
Current Biology, 14, (24), . (doi:10.1016/j.cub.2004.12.036).
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In this paper in volume 14, issue 15 of Current Biology (pp. 1374–1379), we reported experiments on animals derived from the strain RB629 and carrying a deletion in latrophilin, lat-1(ok379). 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. After publication of this work, David Bell reported to us his unpublished observations on RB629. He could not balance lat-1(ok379), nor could he identify animals homozygous for the deletion. We performed further analysis of RB629 and confirmed that animals derived from this strain are emodepside resistant. However, we have also subsequently found that animals derived from 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 conclusions in this regard are invalid. The other substantial findings of the paper, the observation of emodepside resistance in animals treated with RNAi for lat-1 and in mutants for other synaptic proteins, are not affected by this revision.
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