In this Letter, we used strain MT2124, the standard let-60
gf)strain maintained in the Caenorhabditis Genetics Center, forodour-chemotaxis assays. However, we have found that this strain carries a side mutation(s) that profoundly impairs chemotaxis tothe odorant isoamyl alcohol, indicating that we need to re-evaluateour conclusion from the results shown in Fig. 1 that thelet-60(n1046
gf) mutant has a reduced efficiency of odorant chemotaxis.We outcrossed MT2124 to the wild-type N2 and obtained twolet-60(n1046
gf) strains, JN130 and JN131. We also outcrossed theMT4866 strain, the let-60
lf) strain used in the study, andobtained the JN148 strain. All the outcrossed strains show reducedchemotaxis to the two odorants tested, isoamyl alcohol and diacetyl,at low odorant concentrations (T.H. and Y.I., unpublished results).The chemotaxis defects are comparable in extent to, or slightlyweaker than, the original MT4866 let-60
lf) strain. Ourconclusion that both inactivation and hyperactivation of LET-60Ras cause reduced chemotaxis therefore remains unchanged. However,the result shown in Fig. 1d, which suggested that ksr-1
(lf) and mpk-1
(lf) suppress let-60
gf), is no longer validbecause outcrossed let-60
gf) strains do not show chemotaxisdefects at the odorant concentration used in Fig. 1d (1 1023dilution of isoamyl alcohol).
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 Afterpublication of this work, David Bell reported to us his unpublished observations on RB629.He could not balance lat-1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.
The authors, Coleman-Hulbert, AL; Johnson, E; Sedore, CA; Banse, SA; Guo, M2; Driscoll, M3; Lithgow, GJ; and Phillips, PC, submit the following correction for 10.17912/micropub.biology.000131
The original text as read &#8220;We assayed lifespan in response to imatinib mesylate exposure in threeCaenorhabditisspecies in triplicate using our previously published workflow (Lucanicet al. 2017a; b). is correct.
The reference Lucanic 2017b et al. is:
Lucanic M, Driscoll M, Plummer WT, Harke J, Chen E, Bhaumik D, Harinath G, Coleman-Hulbert A, Dumas K, Onken B, Johnson E, Fougler A, Guo S, Crist A, Presley M, Xue J, Sedore C, Chamoli M, Change M, Chen M, Angeli S, Royal MA, Willis J, Edgar D, Shobna P, Chao E, Kamat S, Hope J, Ibanez-Ventoso C, Kish J, Guo M, Phillips P, Lithgow G. Standardized protocols from theCaenorhabditisIntervention Testing Program 2013-2016: Conditions and assays used for quantifying the development, fertility and lifespan of hermaphroditicCaenorhabditisstrains. Protoc. Exch. 2017. doi: 10.1038/protex.2016.086.
The following reference is incorrect:
Plummer WT, Harke J, Lucanic M, Chen E, Foulger AC, Onken B, Coleman-Hulbert AL, Dumas KJ, Guo S, Johnson E, Bhaumik D, Xue J, Crist AB, Presley MP, Harinath G, Sedore CA, Chamoli M, Kamat S, Chen MK, Angeli S, Chang C, Willis JH, Edgar D, Royal MA, Chao EA, Shobna P, Garrett T, Ibanez-Ventoso C, Hope J, Kish JA, Guo M, Lithgow GJ, , Phillips PC. Standardized protocols from the Caenorhabditis Intervention Testing Program 2013-2016: Conditions and assays used for quantifying the development, fertility and lifespan of hermaphroditic Caenorhabditis strains. Protoc. Exch. 2017b. 10.1038/protex.2016.086