<HashMap><database>ENA</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR863/007/SRR8634167/SRR8634167.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR863/008/SRR8634168/SRR8634168.fastq.gz</Fastqsanger.gz></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Genomics</omics_type><center_name>State Key Laboratory of Virology, College of Life Sciences, Wuhan University</center_name><full_dataset_link>https://www.ebi.ac.uk/ena/browser/view/PRJNA524341</full_dataset_link><scientific_name>Drosophila melanogaster</scientific_name><tag>xref:PubMed:30837153</tag><long_description>Drosophila Trf4-1 is a polyadenylation polymerase or terminal nucleotidyl transferase (PAP/TENT) that has been reported to add poly(A) tails to snRNAs in nucleus or mRNAs in cytoplasm. Here, we found that the loss of Trf4-1 resulted in the reduction of mRNAs and primary miRNAs (pri-miRNAs) in both Drosophila S2 cells and adult flies. Interestingly, the role of Trf4-1 in transcription is independent of its PAP/TENT activity. Moreover, using the chromatin immunoprecipitation assay, we uncovered that the loss of Trf4-1 led to abnormal RNA polymerase II accumulation and reduced H3K4me3 binding in promoter regions. Overall design: Small RNA profile of RNAi based knock-down cells</long_description><repository>ENA</repository></additional><is_claimable>false</is_claimable><name>Drosophila Trf4-1 involvement in mRNA and primary miRNA transcription</name><description>Drosophila Trf4-1 involvement in mRNA and primary miRNA transcription</description><dates><last_updated>2025-09-24</last_updated><first_public>2019-05-02</first_public></dates><accession>PRJNA524341</accession><cross_references><GEO>GSE127210</GEO><taxon>7227</taxon><PubMed>30837153</PubMed></cross_references></HashMap>