biostudies-arrayexpressGozde BuyukkahramanHomo sapienshttps://www.ebi.ac.uk/biostudies/studies/E-MTAB-13340Human B lympoblastoid cells, GM12878 and human T cells, JURKAT, were treated with aphidicolin (to arrest cells at G1/S boundary) for 24h, the last 12h with the Sendai virus. The experiment was performed in three biological replicates. Gene expression changes upon aphidicolin and or infection between two cell lines was observed.biostudies-arrayexpressSequencing - 50 bp paired-end sequencing was performed by Illumina Nextseq 2000.Nucleic Acid Extraction - RNA was isolated using RNeasy mini kit (Qiagen) according to manufacturer's instructions. DNA was removed by 2h treatment with TURBO DNase (Thermo Fisher Scientific) and RNA was cleaned up using RNA Clean & Concentrator-25 kit according to the supplier’s instructions (Zymo Research).Sample Collection - At the end of 24 hours, cells were washed with cold 1x PBS twice. Cells were collected in RLT buffer (Qiagen) supplemented with dTT as suggested by RNeasy mini RNA extraction protocol.Growth Protocol - GM12878 and JURKAT cells were cultured with RPMI media supplemented with 10% FBS 37C with 5% CO2.Library Construction - Library prep was performed according to TruSeq® Stranded mRNA kit (Illumina) protocol.Sample Treatment - When cells are 80% confluent, 1 uM of aphidicolin was added to the media and incubated for 12 hours at 37C. Sendai Virus or media was added to the media and incubated for and additional of 12 hours at 37C.OrganizationMINSEQE ScoreAssays and DataProcessed DataMAGE-TAB FilesData Transformation - Raw count matrix was provided. No normalization was performed.MetabolomicsUnknownTranscriptomicsGenomicsProteomicsIllumina HiSeq 2000Interferons (IFNs) have various roles in antiviral immunity, including curbing the immune system to prevent tissue damage and stimulating adaptive immunity. Due to its protective and destructive properties, IFN expression is tightly regulated. In contrast to its tight regulatory control, IFN expression is highly heterogeneous across many cell types upon pathogenic stimulus. The basis for this heterogenous IFN expression remains incompletely understood. Using single cell RNA-sequencing upon viral infection, we found that interferon expression is upregulated specifically in the late G1 phase of the cell cycle, and cell synchronization at the G1/S boundary boosts interferon expression. Furthermore, cell cycle arrest without any additional stimulus is sufficient to upregulate interferons and hundreds of other inflammatory response genes. Interferon upregulation at the G1/S boundary is cell type specific and not observed in non-immune cell types. Finally, we use ATAC-seq to identify potential transcription factors orchestrating this response. Together, these results uncover the cell cycle as a critical regulator of IFN expression in immune cells.RNA-seq of coding RNAHomo sapiensG1/S Boundary Activates Interferon and Inflammatory Response GenesTae Hoon KimGozde BuyukkahramanBuyukkahraman, G. and Kim, T.H.falseRNA-seq of human GM12878 and JURKAT cells treated with aphidicolin and Sendai virus against untreated controlsHuman B lympoblastoid cells, GM12878 and human T cells, JURKAT, were treated with aphidicolin (to arrest cells at G1/S boundary) for 24h, the last 12h with the Sendai virus. The experiment was performed in three biological replicates. Gene expression changes upon aphidicolin and or infection between two cell lines was observed.2025-08-27T00:00:00Z2024-07-30T20:00:41.106Z2023-09-11T21:38:29.368ZE-MTAB-13340ERP151079EFO_0002944EFO_0004170EFO_0003789EFO_0005518EFO_0003816EFO_0003738EFO_0004184EFO_000396910.1101/2023.08.24.554683