Chan, S.-K. and Struhl, G. (2002) Cell 111, 265-280
This paper presents a series of experiments that challenge the
conventional view that Armadillo transduces Wingless by combining
with Pangolin to form a transcriptional activator. The challenge
rests principally on experiments performed by my coauthor, S.-K.
Chan, the results of which are shown in the Figures 2D, 4, and 5.
These experiments test the function of altered forms of Armadillo
that are targeted inside or outside of the nucleus or that contain
heterologous transcriptional activator or repressor domains.
Recently, in seeking to extend these findings, I personally obtained
the opposite result for the key negative control for the experiments
in Figure 5 (Figure 5B). When confronted with this discrepancy, S.-K.
Chan informed me that most of the results shown in Figures 2D, 4, and
5, including the negative control shown in Figure 5B, were either not
performed or gave different results than presented in the paper. I
therefore withdraw this paper and the conclusions it reports. I
deeply regret and apologize for any adverse consequences that may
have resulted from its publication. S.-K. Chan concurs with this
retraction.
Chandok, M.R., Ytterberg, A.J., van Wijk, K.J., and Klessig, D.F.
(2003). Cell 113, 469-482.
The above paper describes the purification and characterization of a
pathogen-inducible NOS-like activity from tobacco plants and its
identification as a variant form of the P subunit of the glycine
decarboxylase complex. The demonstration that recombinant Arabidopsis
variant P protein has NO-synthesizing activity was a critical piece
of evidence leading to the above conclusion. Further experiments by
other members of the Klessig laboratory reveal difficulties in
reproducing the data with recombinant variant P and in addition
suggest that the data on recombinant variant P presented in Tables 1
and 2 and in Figures 5B and 5C of this paper are unreliable. Since we
cannot substantiate the major conclusion presented in this paper, we
wish to retract the entire paper and its conclusions in order to
avoid wasted efforts by other investigators whose studies might be
influenced by the results and conclusions reported. The first author,
M.R. Chandok, has not approved this retraction. We deeply regret that
this serious incident occurred and sincerely apologize to our
colleagues.
Yamaguchi, R. and Newport, J. (2003) Cell 113, 115-125
This paper reports results of experiments that together strongly
support the conclusion that, in metazoan cells, formation of a
complex consisting of the GTP binding protein Ran, the exportin Crm1,
and the DNA helicase MCM plays a critical role in limiting DNA
replication to a single round each cell cycle. This conclusion is
largely based on two experimental results: (1) Experiments which show
that a Ran mutant, RanQ69L, that binds GTP but cannot hydrolyze it
inhibits incorporation of the MCM helicase into pre-replication
complexes (pre-RC's) in Xenopus egg extracts. (2) Equally important
is the observation that addition of a Ran mutant that cannot bind
GTP, Ran T24N, induces both re-binding of MCM helicase to DNA
following a single round of DNA replication and induces a second
round of replication. Together these results suggested that
sequestration of MCM into a Crm1-Ran complex within nuclei during S
phase of the cell cycle functioned to limit replication to a single
round. In the course of pursuing this model further, a postdoctoral
fellow in my laboratory, Dr. Peter Trabold, was able to reproduce
results reported using the RanQ69L mutant. However, he was unable to
reproducibly observe either the substantial reloading of MCM onto DNA
or the robust re-replication reported to occur following addition of
RanT24N. Occasionally, modest excess replication was observed
following addition of RanT24N. However, further investigation
demonstrated that this replication was most likely due to the
transient permeablization of nuclei caused by addition of RanT24N.
Therefore, although experiments using RanQ69L support a model
involving the Crm1-MCM complex to limit re-replication, the inability
of RanT24N to induce re-replication leaves the model unproven. In
light of these new results, I am withdrawing the paper and the
conclusions included in it.
The first author of this article, Ryuji Yamaguchi, is not a coauthor
on this retraction because he stands firmly by the data presented in
the article.