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Transfer RNA pools in human cells are controlled by selective gene expression [ChIP-seq]

ABSTRACT: Transfer RNAs are required for translating genetic information into protein sequence. The human genome contains hundreds of tRNA genes, many of which in multiple copies. How their expression is regulated to control functional tRNA levels is unknown. Here, we combined quantitative tRNA profiling and ChIP-Seq to measure tRNA expression upon differentiation of human induced pluripotent stem cells (hiPSC) into neuronal and cardiac cells. We find that tRNA transcript pools vary substantially, while the abundance of tRNAs with distinct anticodons, which governs decoding rates, is more stable among cell types. Mechanistically, RNA Polymerase III (Pol III) samples a wide range of tRNA genes in hiPSC and becomes constrained to a housekeeping subset upon differentiation. This is mediated by diminished mTOR signaling, which activates the Pol III repressor MAF1. Our data rationalize how tRNA anticodon pools are buffered in different cellular contexts and reveal that mTOR activity drives selective tRNA expression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE227924 | GEO | 2023/10/23

REPOSITORIES: GEO

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Transfer RNA pools in human cells are controlled by selective gene expression [Ribo-seq]

Project description:Transfer RNAs are required for translating genetic information into protein sequence. The human genome contains hundreds of tRNA genes, many of which in multiple copies. How their expression is regulated to control functional tRNA levels is unknown. Here, we combined quantitative tRNA profiling and ChIP-Seq to measure tRNA expression upon differentiation of human induced pluripotent stem cells (hiPSC) into neuronal and cardiac cells. We find that tRNA transcript pools vary substantially, while the abundance of tRNAs with distinct anticodons, which governs decoding rates, is more stable among cell types. Mechanistically, RNA Polymerase III (Pol III) samples a wide range of tRNA genes in hiPSC and becomes constrained to a housekeeping subset upon differentiation. This is mediated by diminished mTOR signaling, which activates the Pol III repressor MAF1. Our data rationalize how tRNA anticodon pools are buffered in different cellular contexts and reveal that mTOR activity drives selective tRNA expression.

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Contrasting effects of whole-body and hepatocyte-specific deletion of the RNA polymerase III repressor Maf1 in the mouse [ChIP-Seq]

Project description:MAF1 is a nutrient-sensitive, TORC1-regulated repressor of RNA polymerase III (Pol III). MAF1 downregulation leads to increased lipogenesis in Drosophila melanogaster, Caenorhabditis elegans, and mice. However, Maf1−/− mice are lean as increased lipogenesis is counterbalanced by futile pre-tRNA synthesis and degradation, resulting in increased energy expenditure. We compared Chow-fed Maf1−/− mice with Chow- or High Fat (HF)-fed Maf1hep−/− mice that lack MAF1 specifically in hepatocytes. Unlike Maf1−/− mice, Maf1hep−/− mice become heavier and fattier than control mice with old age and much earlier under a HF diet. Liver ChIPseq, RNAseq and proteomics analyses indicate increased Pol III occupancy at Pol III genes, very few differences in mRNA accumulation, and protein accumulation changes consistent with increased lipogenesis. Futile pretRNA synthesis and degradation in the liver, as likely occurs in Maf1hep−/− mice, thus seems insufficient to counteract increased lipogenesis. Indeed, RNAseq and metabolite profiling indicate that liver phenotypes of Maf1−/− mice are strongly influenced by systemic inter-organ communication. Among common changes in the three phenotypically distinct cohorts, Angiogenin downregulation is likely linked to increased Pol III occupancy of tRNA genes in the Angiogenin promoter.

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Project description:MAF1 represses Pol III-mediated transcription by interfering with TFIIIB and Pol III. Herein, we found that MAF1 knockdown induced CDKN1A transcription and chromatin looping concurrently with Pol III recruitment. Simultaneous knockdown of MAF1 with Pol III or BRF1 (subunit of TFIIIB) diminished the activation and looping effect, which indicates that recruiting Pol III was required for activation of Pol II-mediated transcription and chromatin looping. ChIP analysis after MAF1 knockdown indicated enhanced binding of Pol III and BRF1, as well as of CFP1, p300, and PCAF, which are factors that mediate active histone marks, along with the binding of TBP and POLR2E to the CDKN1A promoter. Simultaneous knockdown with Pol III abolished these regulatory events. Similar results were obtained for GDF15. Our results reveal a novel mechanism by which MAF1 and Pol III regulate the activity of a protein-coding gene transcribed by Pol II. Knockdown assay was performed using siRNA obtained from MISSION®RNA (Sigma). Inhibition of expression of Pol III (SASI_Hs01_00046568) and MAF1 (SASI_Hs01_00135954) was achieved by transfection with LipofectamineTM RNAiMax (Invitrogen) according to the manufacturer’s protocol. MISSION® siRNA Universal Negative Control (Sigma) was used as knockdown control. Cells were transfected in serum-free medium. After 8 h, the siRNA containing medium was replaced with complete medium.

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