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Vol. 14, No. 2, pp. 198-211, January 15, 2000
1 Department of Zoology and Animal Biology, University of
Geneva, Sciences III, 1211 Geneva 4, Switzerland; 2 National
Institute for Medical Research, London, UK
Transposition of Hoxd genes to a more posterior (5')
location within the HoxD complex suggested that colinearity in
the expression of these genes was due, in part, to the existence of a
silencing mechanism originating at the 5' end of the cluster and
extending towards the 3' direction. To assess the strength and
specificity of this repression, as well as to challenge available
models on colinearity, we inserted a Hoxb1/lacZ
transgene within the posterior HoxD complex, thereby
reconstructing a cluster with a copy of the most anterior gene inserted
at the most posterior position. Analysis of Hoxb1 expression
after ectopic relocation revealed that Hoxb1-specific activity
in the fourth rhombomere was totally abolished. Treatment with retinoic
acid, or subsequent relocations toward more 3' positions in the
HoxD complex, did not release this silencing in hindbrain
cells. In contrast, however, early and anterior transgene expression in
the mesoderm was unexpectedly not suppressed. Furthermore, the
transgene induced a transient ectopic activation of the neighboring
Hoxd13 gene, without affecting other genes of the complex. Such
a local and transient break in colinearity was also observed after
transposition of the Hoxd9/lacZ reporter gene,
indicating that it may be a general property of these transgenes when
transposed at an ectopic location. These results are discussed in the
context of existing models, which account for colinear activation of
vertebrate Hox genes.
[Key Words: Hox gene; transgenes; transposition; expression]
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