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Is the Regulation of Insulin Signaling Multi-Organismal?
Angela E. Douglas (13 December 2011)
Sci. Signal. 4 (203), pe46-pe46. [DOI: 10.1126/scisignal.2002669]
Abstract »   Full Text »  PDF » 
Posted E-Letters:

Noting Two Scientific Inaccuracies

Dear Pr. Douglas,

We have read with interest your recent Perspective in Science Signaling (13th December 2011 issue) that summarizes and comments our recently published papers (Shin et al. Science 334, 670-6744; Storelli et al. Cell Metab. 14, 403-414). While we are completely aware that the "Perspective" format is by essence reflecting the author's opinion, we would like to bring to your attention two scientifically inaccurate statements that might be misleading to the readers and therefore, we believe, should be corrected.

First, at the end of the abstract, the following sentence is written "Different gut bacteria and bacterial effectors were implicated: acetic acid produced by Acetobacter pomorum and branched-chain amino acids produced by Lactobacillus plantarum, respectively". While it is true that both papers implicated different gut bacteria and that Shin et al. showed that the production of acetic acid by A. pomorum is a necessarily (but not sufficient) step in insulin signaling promotion, it is not correct to state that Storelli et al. have implicated L. plantarum-produced branched- chain amino acids in insulin signalling. There is not a single experimental data in the Cell Metabolism paper that support this statement. This is problematic since this personal interpretation and speculation on how L. plantarum might regulate larval growth is presented as a demonstrated fact in the abstract. In contrast, this interpretation is correctly presented in the conditional tense in the core of the text:

"Instead, the key products of L. plantarum may be protein-derived branched chain amino acids, which activate TOR signaling...".

We do not favour this interpretation and actually proposed an alternative scenario that assimilation of diet-derived banched-chain amino acids is enhanced by L. plantarum but this is also a matter of speculation.

Second, in the core of your text (third column, end of first paragraph), the sentence "Storelli et al. obtained unambiguous effects with L. plantarum, which was one of four bacterial species derived from Drosophila guts that Shin et al. reported as supporting larval growth rates no better than germ-free larvae." is inaccurate. In Figure 1B of the Science paper, it is shown that all tested commensal strains (including L. plantarum) upon association do sustain larval development, while germ-free individuals are lethal in the condition tested. Indeed, in this diet condition, A. pomorum is the most efficient bacterial strain to promote growth but L. plantarum can do it also. Of note, on the diet used in the Cell Metabolism paper, A. pomorum is much less efficient (if at all) at promoting larval growth (unpublished data, F.L & J.R). This points to a key impact of the diet on the biology of host/ intestinal bacteria association.

Given the visibility of Science Signaling, these inaccuracies may convey an erroneous perception of our results to a large audience. As corresponding authors of the discussed papers, we feel that it is our duty to contact you regarding this matter in order to get these misquotations corrected. We hope that you will understand our concerns and help us resolving this matter.

With our best regards,

Dr. François Leulier, Pr. Julien Royet, and Pr Won-jae Lee

Editor's Note: In response to this message, Dr. Douglas has corrected the statements identified as inaccurate or misleading and Science Signaling issued an erratum in the 21 February 2012 issue.

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