Ron Wides, a biologist specializing in pattern development at Bar-Ilan University, Israel, and colleagues have retracted a paper published in Mechanisms of Development after his lab found that their technique to delete the Ten-a gene ended up deleting other nearby genes, too.
It was deletions of other genes, and not Ten-a, that killed the fruit flies, Wides concluded. His group had also concluded, erroneously, that Ten-a is what’s known as a “pair-rule” gene. Fruit fly embryos develop in stacked segments, like tubes of Pringles; pair-rule genes guide the development of alternating segments. Those other loci, and not Ten-a, caused lethality and caused the flies to develop improperly early, Wides concluded.
This article has been retracted at the request of the author, for the following reason.
A recently produced deletion mutation of the Drosophila melanogaster gene Ten-a removes the entire gene, yet does not lead to lethality. Thus the lethality and the pair-rule gene roles reported for Ten-a in Mech. Dev., 124 (2007) 911–924 cannot be attributed to this gene, but to second site loci in mutants studied. Given the centrality of the pair-rule claim for this paper, it has been retracted. The other findings of the paper remain as reported, particularly molecular and biochemical characterizations of the Ten-a gene, its alleles and its transcripts.
This seems like a worthy attempt to correct the literature, the kind we generally applaud. There doesn’t seem to have been any misconduct involved.
So we were puzzled when we didn’t hear back from Wides, and when David Wilkinson, the journal’s editor-in-chief, referred our questions to a spokesperson for the journal’s publisher, Elsevier — who in turn declined to comment. That lack of willingness to answer questions always makes us wonder what’s really behind a notice, of course, and we’ll update with anything else we learn.
So in the meantime, we looked into what effects the retraction might have on the field. The paper has been cited eight times, according to Thomson Scientific’s Web of Knowledge, most recently by two papers in Nature in April that appeared here and here.
We contacted Tim Mosca, a co-author of the two Nature papers, to ask what effect the withdrawal might have on the field. In those papers, Mosca and his colleagues found a completely different function for Ten-a than the Wides group originally did. Ten-a and another similar protein Ten-m act together to help information flow from neuron to neuron across what’s known as a synapse — the miniscule gap between neurons — the Stanford group concluded.
Mosca — which means, we feel obligated to note, “fly” in Spanish — said their work did not lead to the Wides retraction. He tells Retraction Watch:
As far as I know (since I am not the person in the lab who made the Ten-a mutant), we made the mutant some time ago just because we identified Ten-a in a nervous system screen and needed a mutant.
For the Stanford group, lethality — aka viability — wouldn’t have become an issue since the researchers deleted the Ten-a gene’s activity from single neurons, and not from the entire fly.
For many of our studies involving mosaic cell analysis, it doesn’t matter if the mutant is non-viable (so that doesn’t factor in for us) since we can remove function specifically in single neurons. That way, we can bypass any organismal need for a specific gene in viability. Fortunately for us, the viability of a fly doesn’t typically hinge on a single olfactory projection or receptor neuron!