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Corrigendum
for
Tian et al.,
First published online September 26, 2008
doi: 10.1242/10.1242/dev.029678
Corrigendum |
There was a reanalysis of data required to support the findings in Development 132, 133-142.
We have repeated the facial analysis reported in Fig. 2 to provide the data required to support some of the original findings of this study (see Publisher's note). Our findings substantiate the original conclusions drawn from Fig. 2 of a dose-related genetic interaction between Disp1 and Shh alleles, and of the function of Disp1 within Shh-producing cells. Some differences are reported below, which might reflect slight differences in embryonic staging or increased sensitivity of the whole-mount in situ hybridization procedure here. Importantly, they do not alter the key conclusion that reducing Disp1 levels in Shh-producing cells results in a phenotype similar to that of genetically matched embryos with reduced Disp1 activity throughout the embryo. These data support the overall conclusions of the paper, and, together with other data in the same report, support a model in which the principal requirement for Disp1 activity is in Shh-producing cells.
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Disp1
2/2C; ShhCre/+ embryos in
which Disp1 activity was specifically knocked down in Shh-producing
cells have a facial phenotype with a narrowing of the face and reduction of
the premaxilla. However, the length of the snout is similar to wild type and
the mandibular incisors are not fused (Fig.
2A,C,K,M). Thus, the phenotype is, as expected, generally less
severe than that of the Disp12/2;
Shh+/- embryos (Fig.
2B,L). The severity of the conditional phenotype is enhanced when
Disp1 activity is further lowered in
Disp12C/C829F; ShhCre/+ mice
(Fig. 2E,O) but the phenotype
is slightly weaker than that in Disp12/C829F (data
not shown) or Disp12/C829F; Shh+/-
embryos (Fig. 2D,N); the
tubular nasal process was shorter and the premaxillary bone was more
extensive. In a proportion of the latter, truncated fused mandibles lack
incisors (Fig. 2N); however,
mandibular fusion was not observed in Disp12C/C829F;
ShhCre/+ embryos. The slightly weaker facial phenotype seen at
term with each of the conditional removal combinations was evident at E10.5
when the distance between the Fgf8-expressing frontal-nasal processes
is compared by whole-mount in situ hybridization
(Fig. 2F-J). Variable weak
midline Shh expression was observed rostral to the optic stalk in
Disp12/2C; ShhCre/+ embryos at
E9.5 (Fig. 2U-W). As expected,
this resulted in Ptch1 expression in adjacent nascent facial
structures (Fig. 2P-R). Small,
weak domains of Shh and Ptch1 expression were observed close
to the midline, localized to the region of the optic stalk in
Disp12C/C829F; ShhCre/+ embryos (not
readily visible in Fig. 2T,Y).
Only Disp12/C829F; Shh+/- embryos, the
strongest genetic combination, completely lacked Shh and
Ptch1 expression rostral to the diencephalon
(Fig. 2S,X).
The authors apologise to readers for any inconvenience caused by the requirement to replicate these data and thank Mary Duah and Jill McMahon for replicating the experiments, Joe Vaughan and Celia Shneider for help with data acquisition, Renate Hellmiss for generating the figures and the journal Development for encouraging the reanalysis.
Publisher's note
Re: Tian, H., Jeong, J., Harfe, B. D., Tabin, C. J. and McMahon, A. P. (2005a). Mouse Disp1 is required in sonic hedgehog-expressing cells for paracrine activity of the cholesterol-modified ligand. Development 132, 133-142.
In 2005, the McMahon laboratory reported that a re-examination of two
papers published by their group in Development
(Tian et al., 2004
;
Tian et al., 2005a) had
revealed a duplication of Dr Tian's data in these papers. Following their
analysis, the authors announced, with regret, that they must retract Tian et
al. (2004), and this retraction
was published by Development in November 2005, along with their
apology to the editors and readership of the journal
(Tian et al., 2005b). With
respect to the second paper (Tian et al.,
2005a), the authors' review, overseen by the Committee on
Professional Conduct (CPC) for the Faculty of Arts and Sciences at Harvard
University, found that the principal conclusions of the paper were supported
by appropriate documentation but that the documentation for
Fig. 2 was inadequate,
requiring a replication of those data. The replicated data have been reviewed
by Development and are published in this Corrigendum.
Development and its publishers take very seriously issues relating to
the authenticity of data. We acknowledge the dedication and openness of the
McMahon laboratory in this matter, and the contributions of additional members
of the laboratory, not on the paper's authorship list, in repeating these
extensive experiments and data analyses for the Corrigendum.
REFERENCES
Tian, H., Tenzen, T. and McMahon, A. P. (2004).
Dose dependency of Disp1 and genetic interaction between
Disp1 and other hedgehog signaling components in the mouse.
Development 131,4021
-4033.
Tian, H., Jeong, J., Harfe, B. D., Tabin, C. J. and McMahon, A.
P. (2005a). Mouse Disp1 is required in sonic
hedgehog-expressing cells for paracrine activity of the cholesterol-modified
ligand. Development 132,133
-142.
Tian, H., Tenzen, T. and McMahon, A. P.
(2005b). Retraction: Dose dependency of Disp1 and
genetic interaction between Disp1 and other hedgehog signaling
components in the mouse. Development
132, 5615.
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