Post-transcriptional regulation of proliferation and quiescence
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ABSTRACT:
PROVIDER: PRJNA744468 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15058840.fastq.gz | Fastqsanger.gz | |||
| SRR15058841.fastq.gz | Fastqsanger.gz | |||
| SRR15058842.fastq.gz | Fastqsanger.gz | |||
| SRR15058843.fastq.gz | Fastqsanger.gz | |||
| SRR15058844.fastq.gz | Fastqsanger.gz |
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Project description:Several studies have reported that functionally related genes exhibit similar codon usage, which has been shown to impact protein production by the control of mRNA decay or translation. However, codon-mediated control and their relationship to growth conditions have been intensely debated and remain unclear. Here, we investigate the post-transcriptional gene expression control mechanisms employed in cells in proliferation or quiescence. These investigations show that in proliferative conditions we see that subsets of mRNAs with increased mRNA stability are associated with enhanced translation. However, this is not the case in quiescence, where mRNA stability is not linked to changes in translation. In addition, we observe that while G/C-ending codons are more frequently used in both conditions, there is a shift towards A/U-ending codons in proliferation, and this is accompanied by corresponding changes in tRNAs and translational output.
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Project description:To survive in nutrient-poor conditions, cells must exit the cell cycle and enter a reversible non-replicative state known as quiescence. Yeast cells reprogram their gene expression during quiescence entry to silence transcription, but how the nascent transcriptome changes in quiescence has not been determined. By investigating the nascent transcriptome in quiescent yeast cells, we found noncoding transcription represented a larger portion of the quiescent transcriptome than in G1. To enable our nascent transcriptome analyses, we annotated over a thousand noncoding RNAs (ncRNAs) in quiescence and G1. Our work revealed that both mRNA and ncRNA are subject to increased post-transcriptional regulation in quiescence compared to G1. We found that the nuclear exosome-NNS pathway suppresses over one thousand mRNAs, in addition to canonical noncoding RNAs, in quiescence. In quiescence, a minority of the mRNAs affected by the NNS-nuclear exosome pathway are the same as those identified when glucose was removed, demonstrating a previously unidentified role for the pathway. RNA sequencing through the diauxic shift revealed at least two distinct time points at which the nuclear exosome controls the abundance of mRNAs involved in protein production, cellular organization, and metabolism, for optimal quiescence entry. Both transcription and post-transcriptional regulation are dramatically reprogrammed in quiescence, shifting the balance of noncoding and coding transcripts. The nuclear exosome and NNS are crucial for proper regulation of both mRNAs and ncRNAs in quiescence and through quiescence entry.
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Project description:Cells switch between quiescence and proliferation states for maintaining tissue homeostasis and regeneration. At the restriction point (R-point), cells become irreversibly committed to the completion of the cell cycle independent of mitogen. The mechanism involving hyper-phosphorylation of retinoblastoma (Rb) and activation of transcription factor E2F is linked to the R-point passage. However, stress stimuli trigger exit from the cell cycle back to the mitogen-sensitive quiescent state after Rb hyper-phosphorylation but only until APC/CCdh1 inactivation. In this study, we developed a mathematical model to investigate the reversible transition between quiescence and proliferation in mammalian cells with respect to mitogen and stress signals. The model integrates the current mechanistic knowledge and accounts for the recent experimental observations with cells exiting quiescence and proliferating cells. We show that Cyclin E:Cdk2 couples Rb-E2F and APC/CCdh1 bistable switches and temporally segregates the R-point and the G1/S transition. A redox-dependent mutual antagonism between APC/CCdh1 and its inhibitor Emi1 makes the inactivation of APC/CCdh1 bistable. We show that the levels of Cdk inhibitor (CKI) and mitogen control the reversible transition between quiescence and proliferation. Further, we propose that shifting of the mitogen-induced transcriptional program to G2-phase in proliferating cells might result in an intermediate Cdk2 activity at the mitotic exit and in the immediate inactivation of APC/CCdh1. Our study builds a coherent framework and generates hypotheses that can be further explored by experiments.
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Project description:The reactivation of quiescent cells to proliferate is fundamental to tissue repair and homeostasis in the body. Often referred to as the G0 state, quiescence is however not a uniform state but with graded depth. Shallow quiescent cells exhibit a higher tendency to revert to proliferation than deep quiescent cells, while deep quiescent cells are still fully reversible under physiological conditions, distinct from senescent cells. Cellular mechanisms underlying the control of quiescence depth and the connection between quiescence and senescence are poorly characterized, representing a missing link in our understanding of tissue homeostasis and regeneration. Here we measured transcriptome changes as rat embryonic fibroblasts moved from shallow to deep quiescence over time in the absence of growth signals. We found that lysosomal gene expression was significantly upregulated in deep quiescence, and partially compensated for gradually reduced autophagy flux. Reducing lysosomal function drove cells progressively deeper into quiescence and eventually into a senescence-like irreversibly arrested state; increasing lysosomal function, by lowering oxidative stress, progressively pushed cells into shallower quiescence. That is, lysosomal function modulates graded quiescence depth between proliferation and senescence as a dimmer switch. Lastly, we found that a gene expression signature developed by comparing deep and shallow quiescence in fibroblasts can correctly classify a wide array of senescent and aging cell types in vitro and in vivo, suggesting that while quiescence is generally considered to protect cells from irreversible arrest of senescence, quiescence deepening likely represents a common transition path from cell proliferation to senescence, related to aging.
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