TitleRegulation of Psc-Su(z)2 genes in drosophila melanogaster
NamePark, Sung-Yeon (author), Steward, Ruth (chair), Grant, Barth (internal member), Pirrotta, Vincenzo (internal member), Mckim, Kim (outside member), Rutgers University, Graduate School - New Brunswick,
DescriptionThe Psc and Su(z)2 genes belong to the Polycomb Group (PcG) and Psc itself is one of the core components of the PRC1 repressive complex and genetic evidence suggests that it is autoregulated by PcG mechanisms. Recently, the Psc-Su(z)2 region was also found to contain several putative Polycomb Response Elements that bind PcG proteins while the entire region is enriched for H3K27me3. Current model of PcG mechanism is all-or- none silencing paradigm derived from its role in homeotic gene regulation. However, it is likely that PcG regulation at many other target genes functions by down-regulating rather than silencing expression. This is certainly the case for PcG genes like Psc and Su(z)2. To understand how PcG mechanisms down-regulate a target gene, the nature of the PcG binding sites in the Psc-Su(z)2 region and their repressive effects were analyzed, using reporter gene construct. There are at least two functional PREs that can silence a reporter gene in a PcG-dependent manner and one of them can also show anti-silencing activity, depending on the chromosomal context. In addition, we found a down-regulation module in the vicinity of Psc promoter, whose effect is insensitive to the dosage of PcG genes. Probably, several different regulatory elements might be cooperative to down-regulate Psc-Su(z)2 genes by PcG mechanism. I have also generated small deletions that remove one such binding peak. Deletion of one of the Psc-Su(z)2 PREs increases the expression level of Psc and Su(z)2 by 2-3 fold at late embryonic stage. Perhaps the increased expression of PSC can partially compensate by binding to the other PREs in the Psc-Su(z)2 locus. On the contrary, the expressions of CG13323 and CG13324 genes behind of the PRE are decreased by 20 to 50 fold during entire embryonic stages. Also, the chromatin IP experiment showed that the loss of this fragment extends the domain of H3K27me3 around 10kb further, to a region that includes both of CG13323 and CG13324 transcripts. So, the fragment removed in both deletions may not possess only PRE but also a transcriptional enhancer for downstream genes or boundary element to block the PcG silencing.
NoteIncludes bibliographical references (p. 92-99)
Noteby Sung-Yeon Park
CollectionGraduate School - New Brunswick Electronic Theses and Dissertations
Organization NameRutgers, The State University of New Jersey
RightsThe author owns the copyright to this work.