In situ dissection of the Fab-7 region of the bithorax complex into a chromatin domain boundary and a Polycomb-response element

Jozsef Mihaly, Ilham Hogga, Janos Gausz, H. Gyurkovics, François Karch

Research output: Article

162 Citations (Scopus)

Abstract

Parasegmental (PS)-specific expression of the homeotic genes of the bithorax-complex (BX-C) appears to depend upon the subdivision of the complex into a series of functionally independent cis-regulatory domains. Fab-7 is a regulatory element that lies between iab-6 and iab-7 (the PS11- and PS12-specific cis-regulatory domains, respectively). Deletion of Fab-7 causes ectopic expression of iab-7 in PS11 (where normally only iab-6 is active). Two models have been proposed to account for the dominant Fab-7 phenotype. The first considers that Fab-7 functions as a boundary element that insulates iab-6 and iab-7. The second model envisages that Fab-7 contains a silencer element that keeps iab-7 repressed in parasegments anterior to PS12. Using a P-element inserted in the middle of the Fab-7 region (the bit transposon), we have generated an extensive collection of new Fab-7 mutations that allow us to subdivide Fab-7 into a boundary element and a Polycomb-respond element (PRE). The boundary lies within 1 kb of DNA on the proximal side of the bit transposon (towards iab-6). Deletions removing this element alone cause a complex gain- and loss-of-function phenotype in PS11; in some groups of cells, both iab-6 and iab-7 are active, while in others both iab-6 and iab-7 are inactive. Thus, deletion of the boundary allows activating as well as repressing activities to travel between iab-6 and iab-7. We also provide evidences that the boundary region contains an enhancer blocker element The Polycomb-response element lies within 0.5 kb of DNA immediately distal to the boundary (towards iab-7). Deletions removing the PRE alone do not typically cause any visible phenotype as homozygotes. Interestingly, weak ectopic activation of iab-7 is observed in hemizygous PRE deletions, suggesting that the mechanisms that keep iab-7 repressed in the absence of this element may depend upon chromosome pairing. These results help to reconcile the previously contradictory models on Fab-7 function and to shed light on how a chromatin domain boundary and a nearby PRE concur in the setting up of the appropriate PS-specific expression of the Abd-B gene of the BX-C.

Original languageEnglish
Pages (from-to)1809-1820
Number of pages12
JournalDevelopment
Volume124
Issue number9
Publication statusPublished - máj. 1997

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Response Elements
Insulator Elements
Chromatin
Dissection
Phenotype
Transcriptional Silencer Elements
Chromosome Pairing
Homeobox Genes
DNA
Homozygote
Mutation
Genes

ASJC Scopus subject areas

  • Anatomy
  • Cell Biology

Cite this

In situ dissection of the Fab-7 region of the bithorax complex into a chromatin domain boundary and a Polycomb-response element. / Mihaly, Jozsef; Hogga, Ilham; Gausz, Janos; Gyurkovics, H.; Karch, François.

In: Development, Vol. 124, No. 9, 05.1997, p. 1809-1820.

Research output: Article

Mihaly, Jozsef ; Hogga, Ilham ; Gausz, Janos ; Gyurkovics, H. ; Karch, François. / In situ dissection of the Fab-7 region of the bithorax complex into a chromatin domain boundary and a Polycomb-response element. In: Development. 1997 ; Vol. 124, No. 9. pp. 1809-1820.
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AU - Gyurkovics, H.

AU - Karch, François

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