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GENETIC AND BIOCHEMICAL ANALYSIS OF THE ROLE OF EXTRA SEX COMBS-LIKE IN POLYCOMB SILENCING IN DROSOPHILA MELANOGASTER
| Title: | GENETIC AND BIOCHEMICAL ANALYSIS OF THE ROLE OF EXTRA SEX COMBS-LIKE IN POLYCOMB SILENCING IN DROSOPHILA MELANOGASTER |
| Author: | Kurzhals, Rebeccah Lynn |
| Description: | Maintenance of gene expression states is important for cellular differentiation during development. Chromatin mediates the faithful propagation of expression states, but the exact mechanism of how this occurs is unknown. Drosophila development provides an excellent model to study the maintenance of silenced transcription states. Homeotic gene expression domains are established early in development by transiently expressed repressors. The products of the Polycomb group (PcG) genes maintain gene silencing of the homeotic genes outside of their normal expression domains for the rest of development. The Polycomb group proteins ESC and E(Z) are required for Polycomb silencing. ESC has the distinction of being required only in early development in contrast to other PcG gene products. More recently E(Z) was shown to be a histone methyltransferase (HMTase) and its activity is required continuously throughout development. E(Z) activity is dependent on its association with ESC. This implies that either E(Z) HMTase activity in vivo is not as dependent on ESC or another protein replaces the function of ESC later in development. Here I describe a new PcG gene, extra sex combs-like (escl), a paralog of esc, that encodes the ESCL protein. ESCL is expressed throughout development in contrast to ESC. I demonstrate that ESCL interacts with E(Z) like ESC and that ESCL is associated with components of the embryonic ESC-E(Z) complex in embryogenesis and in larvae when ESC is no longer detectable. E(Z) dependent methylation of histones is absent when both ESC and ESCL are removed demonstrating that either ESC or ESCL is required for histone H3 K27 methylation. A mutation in escl enhances the phenotypes of esc mutants. I demonstrate that over-expression of ESCL rescues esc mutant phenotypes and over-expression of ESCL can functionally substitute for ESC. The findings described in this thesis resolve the paradox that ESC is only required and expressed early in embryogenesis, but ESC is continuously required for the HMTase activity of E(Z). I propose that ESCL replaces ESC later in development in E(Z) complexes required for the continued maintenance of Polycomb silencing. |
| Permanent Link: |
http://rave.ohiolink.edu/etdc/view?acc_num=case1143484105
http://hdl.handle.net/2374.OX/17539 |
| Date: | 2006 |
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