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RNA polyadenylation and cellular ATP levels regulate the stability of RNAs in Escherichia coli

ABSTRACT: To investigate the extent of the effect of poly(A) polymerase (PAP I)-mediated polyadenylation on RNA stability, we performed the first genome-wide study of RNA stability in the absence of PAP I activity. Inactivation of the pcnB gene coding for PAP I led to a global stabilization of E. coli RNAs, with 1403 stabilized transcripts and only 4 destabilized. Stabilized RNAs were involved in essential cellular functions such as DNA replication and repair, translation, RNA degradation, central carbon metabolism but also in stress responses. Because PAP I is an ATP-consuming enzyme we wondered whether the RNA stabilization observed after inactivation of PAP I could also be related to changes in intracellular ATP levels. We demonstrated for the first time in E. coli, that lowering intracellular ATP levels below 1 µM/OD stabilizes RNAs. Although the ATP level was reduced by 20 % in the pcnB mutant on glucose, the ATP level was still too high to have any role in the observed RNA stabilization. However, in experiments where the ATP level was artificially strongly decreased, inactivation of PAP I by substrate availability was implicated in the stabilization mechanism of certain RNAs. This study clearly demonstrates that PAP I is at the crossroads of the regulation of RNA stability by energy status in E. coli cells.

ORGANISM(S): Escherichia coli

PROVIDER: GSE248472 | GEO | 2024/11/27

REPOSITORIES: GEO

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Project description:Heldt2012 - Influenza Virus Replication The model describes the life cycle of influenza A virus in a mammalian cell including the following steps: attachment of parental virions to the cell membrane, receptor-mediated endocytosis, fusion of the virus envelope with the endosomal membrane, nuclear import of vRNPs, viral transcription and replication, translation of the structural viral proteins, nuclear export of progeny vRNPs and budding of new virions. It also explicitly accounts for the stabilization of cRNA by viral polymerases and NP and the inhibition of vRNP activity by M1 protein binding. In short, the model focuses on the molecular mechanism that controls viral transcription and replication. This model is described in the article: Modeling the intracellular dynamics of influenza virus replication to understand the control of viral RNA synthesis. Heldt FS, Frensing T, Reichl U. J Virol. Abstract: Influenza viruses transcribe and replicate their negative-sense RNA genome inside the nucleus of host cells via three viral RNA species. In the course of an infection, these RNAs show distinct dynamics, suggesting that differential regulation takes place. To investigate this regulation in a systematic way, we developed a mathematical model of influenza virus infection at the level of a single mammalian cell. It accounts for key steps of the viral life cycle, from virus entry to progeny virion release, while focusing in particular on the molecular mechanisms that control viral transcription and replication. We therefore explicitly consider the nuclear export of viral genome copies (vRNPs) and a recent hypothesis proposing that replicative intermediates (cRNA) are stabilized by the viral polymerase complex and the nucleoprotein (NP). Together, both mechanisms allow the model to capture a variety of published data sets at an unprecedented level of detail. Our findings provide theoretical support for an early regulation of replication by cRNA stabilization. However, they also suggest that the matrix protein 1 (M1) controls viral RNA levels in the late phase of infection as part of its role during the nuclear export of viral genome copies. Moreover, simulations show an accumulation of viral proteins and RNA toward the end of infection, indicating that transport processes or budding limits virion release. Thus, our mathematical model provides an ideal platform for a systematic and quantitative evaluation of influenza virus replication and its complex regulation. With the current parameter set, the model reproduces an infection at a multiplicity of infection (MOI) of 10. Figure 2A of the paper is reproduced here, with parameters kDegRnp and kSynP changed to zeros. Initial conditions and parameter changes that were used to obtain specific figures in the article can be found in Table A2. The model has the correct value for kAttLo as 4.55e-04. The value of this parameter mentioned as 4.55e-02 in Table 1 of the paper is incorrect. This is checked with the author. This model is hosted on BioModels Database and identified by: MODEL1307270000 . To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models . To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

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RNA polyadenylation and cellular ATP levels regulate the stability of RNAs in Escherichia coli

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