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Ten different Polycomb group genes are required for spatial control of the abdA and AbdB homeotic products

Simon, Jeffrey, Chiang, Anne, Bender, Welcome·1992·Development

Abstract

Mutations in genes of the Polycomb (Pc) group cause abnormal segmental development due to ectopic expression of the homeotic products of the Antennapedia and bithorax complexes. Here the requirements for Pc group genes in controlling the abdA and AbdB products of the bithorax complex are described. Embryos containing mutations in the genes Polycomb (Pc), extra sex combs (esc), Enhancer of zeste [E(z)], polyhomeotic (ph), Sex comb on midleg (Scm), Polycomb-like (Pcl), Sex comb extra (See), Additional sex combs (Asx), Posterior sex combs (Psc) and pleiohomeotic (pho) were examined. In every case, both abdA and AbdB are expressed outside of their normal domains along the anterior-posterior (A–P) axis, consistent with these Pc group products acting in a single pathway or molecular complex. The earliest detectable ectopic expression is highest in the parasegments immediately adjacent to the normal expression boundary. Surprisingly, in the most severe Pc group mutants, the earliest ectopic AbdB is distributed in a pair-rule pattern. At all stages, ectopic abdA in the epidermis is highest along the anterior edges of the parasegments, in a pattern that mimics the normal abdA cell-specific pattern. These examples of highly patterned mis-expression show that Pc group mutations do not cause indiscriminate activation of homeotic products. We suggest that the ectopic expression patterns result from factors that normally activate abdA and AbdB only in certain parasegments, but that in Pc group mutants these factors gain access to regulatory DNA in all parasegments.

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Crossref · 10.1242/dev.114.2.493

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Metadata

Authors
Simon, J., Chiang, A., & Bender, W.
Venue
Development
Published
1992-02-01
Volume
114
Issue
2
Pages
493-505
ISSN
  • 0950-1991 (ISSN-L)
  • 1477-9129
OpenAlex
W1855977133
Cited by
304
References
2
FWCI
6.74
Type
journal article
Language
en
Open access
closed

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