The Coiled Spring How Life Begins by Ethan Bier
Author:Ethan Bier [Bier, Ethan]
Language: eng
Format: epub
Tags: aVe4EvA
Published: 2011-05-21T16:57:58+00:00
■ Chordin Versus BMP4 ■
A series of very elegant experiments conducted in the laboratory of Eddy de Robertis at UCLA, where the chordin gene was isolated, suggested that Chordin functioned by a double-negative mechanism to overcome the antineuralizing activity of BMP4. His lab also showed that Chordin binds to BMP4 and prevents it from activating its receptor. Thus, it became apparent that Chordin, like Sog, promotes neural development indirectly by blocking the neural suppressive activity of BMP4. An experiment that confirmed this hypothesis and brought very satisfying closure to the vertebrate neural inducer field was performed in Hemmati-Brivanlou’s laboratory at Rockefeller University. This group repeated the classic ectoderm dissociation experiment discussed above with the modification of adding identified molecules to the cell culture medium (Fig. 5.4). Hemmati-Brivanlou reasoned that in the original experiments, dissociated ectoderm cells were unable to inhibit one another from assuming the default neural state because the BMP4 they were producing was being greatly diluted by the large volumes of media in which they were incubated. As a consequence of this dilution factor, cells received insufficient levels of BMP4 to be prevented from becoming neurons. To test this idea, he added soluble purified BMP4 to the media into which the cells were dissociated. When these BMP4-treated cells were then reaggregated by centrifugation, they became epidermal rather than neural. He took the experiment yet one step further by showing that if Chordin was added to the media along with BMP4, the reaggregated cells once again became neural. These experiments reversed more than 50 years of thinking and established the current view that the default state of ectoderm in vertebrates as well as invertebrates is neural and that the derived epidermal cell state is dependent on active signaling (i.e., by BMP4/Dpp).
The fact that corresponding genes in flies and frogs perform the same When I was a grad-
functions in D/V patterning led Eddy De Robertis and his collaborators, uate student, the embryonic cell dis-
as well as my own group and our collaborator David Kimelman at the
sociation was actu-
University of Washington, to test the possibility that Dpp and Sog could
ally used as an ex-
pattern the D/V axis of frog embryos. We believed that these experi
ample of how one
ments were unlikely to succeed a priori, given the enormous evolu
had to be very
tionary chasm between vertebrates and invertebrates, but we were mo
careful when de
tivated to try them anyway, partially because of the stunning success
signing an experi
of the previously described McGinnis experiment which demonstrated
ment to avoid gen
that mouse Hox genes can function as their fly counterparts in flies. In erating artifactual
addition, Richard Padgett, while working with Bill Gelbart (the discov- results due to ex
erer of the dpp gene), had shown that a human version of the Dpp gene perimental manip
could substitute for dpp in flies. Even with these encouraging indica- ulations. It is
tions, it seemed to be asking quite a bit to recreate an entire D/V pat-somewhat ironic that this well-cho
terning system in frogs using fly genes.
sen example of an
Pursuing this idea, Kimelman’s group injected sog
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