Poster: Transcription Regulation
Abs #
1031: Replication inhibitor interference with phas promoter activation
In our previous studies, we have shown that the inactive chromatin architecture over the phas promoter in vegetative tissues can be modified and thereby potentiated for transcription by ectopically expressed transcription factor PvALF. Subsequently, transcriptional activation requires the application of exogenous ABA (Li et al., 1998, Li and Hall, 1999). To gain insight to chromatin modification by PvALF, we have evaluated the possibility that DNA replication may provide an avenue for the activator to gain access to the promoter. DNA replication inhibitors, such as hydroxyurea and mimosine, were able to inhibit PvALF and ABA- mediated activation of the phas promoter. However, inhibition of replication following the ectopic expression of PvALF led to a decrease in ABA-mediated activation. This shows that DNA replication affects the activation step and not the potentiation step. The decrease in phas activation upon inhibition of DNA replication can be correlated with a concomitant reduction in transcript abundance for abi5, a transcription activator that is a crucial component of the ABA signal transduction pathway. Using in vitro nucleosome reconstitution studies, it is possible to obtain further insight to the mode of interaction of PvALF with promoter DNA in a naked or a nucleosomal configuration. Changes in histone modifications associated with the activation steps affected by PvALF and ABA are also being evaluated. Supported by NSF Grant MCB-9974706
