More specifically, the announcement of a mutation that is able to generate additional limbs shows that such limbs are actually associated to a duplication of the entire body axis, with the corresponding movements of engulfment and segmentation which create the normal limb plates .
Where  is All-trans retinoic acid-induced ectopic limb and caudal structures: murine strain sensitivities and pathogenesis, Liao X, Collins MD, Dev Dyn. 2008 Jun;237(6):1553-64, doi: 10.1002/dvdy.21568 :
Treatment of pregnant mice at the egg cylinder stage with retinoic acid (RA) has caused ectopic hindlimbs in the offspring. Proposed causes of ectopic hindlimbs include homeotic transformation or multiple axis formation. Two mouse strains were determined to be divergent in susceptibility to this malformation (C57BL/6N, highly sensitive; SWV/Fnn, less sensitive). Ectopic limbs were hindlimbs (expressing Pitx1 and Tbx4 but not Tbx5), yet they also expressed the predominantly forelimb Hoxb8. Ectopic body axis formation was indicated by gene expression for ectopic primitive streaks, notochords, and nodes, as well as inhibition of anterior visceral endoderm and mesodermal migration. The earlier in development that embryos were examined, the higher the rate of ectopic hindlimb development and axis formation. Ectopic axis formation and cell migration inhibition had the same strain susceptibility as the dysmorphogenesis. We propose that all extra hindlimbs were derived from ectopic axis formation, perturbation of which is genetic background dependent.
Fleury got it wrong about the “mutation” and got it wrong about the “duplication of the entire body axis“.
I’m not discussing the “mutation” which corresponds to intoxication by all-trans retinoic acid. One should read at least the titles of the articles he cites.
From the discussion of , Liao & Collins:
The varying degrees of body axis duplication could explain the morphological diversity of hindlimb duplications. It seems that complete anteroposterior body axis duplication, observed in some instances between GD 8.0 and GD 9.0, was incompatible with survival of the embryo because this phenotype was never observed at GD 11. What was compatible with life was an incomplete duplication of the posterior body axis. The degree of posterior body axis duplication could range from a fully formed ectopic primitive streak to a small region of ectopic primitive streak that was only detectable by expression of genetic markers, such as Tbx6, Shh, Foxa2, Brachyury, and Fgf8.
Well, I wouldn’t even discuss duplications of the entire body axis.
And I’ll send Fleury’s conclusions to the incinerator with the dead mice.
But let’s keep one of the experimental results in note for later discussion: the susceptibility of the two strains tested to retinoic acid intoxication is differential.
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