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ELAV ChIP-seq in Drosophila melanogaster embryos

ABSTRACT: Alternative polyadenylation (APA) has been implicated in a variety of developmental and disease processes, such as stem cell differentiation and cancer. A particularly dramatic form of APA has been documented in the developing nervous system of flies and mammals, whereby a variety of neurogenic genes undergo coordinate extension of their 3’ UTRs. In Drosophila, the RNA-binding protein ELAV inhibits RNA processing at proximal polyadenylation (poly(A)) sites, thereby fostering the formation of 3’ extensions that can reach 12 kb in length. Here, we present evidence that paused Pol II plays an important role in the selective recruitment of ELAV to elongated genes. Replacing native promoters of elongated genes with heterologous promoters blocks normal 3’ extension in the nervous system, while native promoters can induce 3’ extension in ectopic tissues expressing ELAV. Computational analyses suggest that the promoter regions of elongated genes tend to contain paused Pol II and associated cis-regulatory elements such as GAGA. ELAV ChIP-Seq assays indicate pervasive binding to the promoter regions of extended genes. Our study provides the first evidence for a regulatory link between promoter-proximal pausing and APA.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE63323 | GEO | 2014/11/21

SECONDARY ACCESSION(S): PRJNA267499

REPOSITORIES: GEO

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ELAV ChIP-seq in Drosophila melanogaster embryos

Project description:Alternative polyadenylation (APA) has been implicated in a variety of developmental and disease processes, such as stem cell differentiation and cancer. A particularly dramatic form of APA has been documented in the developing nervous system of flies and mammals, whereby a variety of neurogenic genes undergo coordinate extension of their 3’ UTRs. In Drosophila, the RNA-binding protein ELAV inhibits RNA processing at proximal polyadenylation (poly(A)) sites, thereby fostering the formation of 3’ extensions that can reach 12 kb in length. Here, we present evidence that paused Pol II plays an important role in the selective recruitment of ELAV to elongated genes. Replacing native promoters of elongated genes with heterologous promoters blocks normal 3’ extension in the nervous system, while native promoters can induce 3’ extension in ectopic tissues expressing ELAV. Computational analyses suggest that the promoter regions of elongated genes tend to contain paused Pol II and associated cis-regulatory elements such as GAGA. ELAV ChIP-Seq assays indicate pervasive binding to the promoter regions of extended genes. Our study provides the first evidence for a regulatory link between promoter-proximal pausing and APA. ELAV ChIP-Seq assays were conducted with nuclei obtained from 6-8 hr and 10-12 hr embryos

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Project description:Control of RNA transcription is critical for the development and homeostasis of all organisms, and can occur at multiple steps of the transcription cycle, including RNA polymerase II (Pol II) recruitment, initiation, promoter-proximal pausing, and elongation. That Pol II accumulates on many promoters in metazoans implies that steps other than Pol II recruitment are rate-limiting and regulated 1-6. By integrating genome-wide Pol II chromatin immunoprecipition (ChIP) and Global Run-On (GRO) genomic data sets from Drosophila cells, we examined critical features of Pol II near promoters. The accumulation of promoter-proximal polymerase is widespread, occurring on 70% of active genes; and unlike elongating Pol II within the body of genes, promoter Pol II are held paused by factors like NELF, unable to transcribe unless nuclei are treated with strong detergent. Notably, we find that the vast majority of promoter-proximal Pol II detected by ChIP are paused, thereby identifying the biochemical nature of this rate-limiting step in transcription. Finally, we demonstrate that Drosophila promoters do not have the upstream divergent Pol II that is seen so broadly and prominently on mammalian promoters. We postulate this is a consequence of Drosophila’s extensive use of directional core promoter sequence elements, which contrasts with mammals’ lack of directional elements and prevalence of CpG island core promoters. In support of this idea, we show that the fraction of mammalian promoters containing a TATA box core element is dramatically depleted of upstream divergent transcription. ChIP-seq data set for Pol II (rpb3) (2 replicates).

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