2,081 research outputs found

    The habitability of the Universe through 13 billion years of cosmic time

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    The field of astrobiology has made tremendous progress in modelling galactic-scale habitable zones which offer a stable environment for life to form and evolve in complexity. Recently, this idea has been extended to cosmological scales by studies modelling the habitability of the local Universe in its entirety (e.g. Dayal et al. 2015; Li & Zhang 2015). However, all of these studies have solely focused on estimating the potentially detrimental effects of either Type II supernovae (SNII) or Gamma Ray Bursts (GRBs), ignoring the contributions from Type Ia supernovae (SNIa) and active galactic nuclei (AGN). In this study we follow two different approaches, based on (i) the amplitude of deleterious radiation and (ii) the total planet-hosting volume irradiated by deleterious radiation. We simultaneously track the contributions from the key astrophysical sources (SNII, SNIa, AGN and GRBs) for the entire Universe, for both scenarios, to determine its habitability through 13.8 billion years of cosmic time. We find that SNII dominate the total radiation budget and the volume irradiated by deleterious radiation at any cosmic epoch closely followed by SNIa (that contribute half as much as SNII), with GRBs and AGN making up a negligible portion (<1%). Secondly, as a result of the total mass in stars (or the total number of planets) slowly building-up with time and the total deleterious radiation density, and volume affected, falling-off after the first 3 billion years, we find that the Universe has steadily increased in habitability through cosmic time. We find that, depending on the exact model assumptions, the Universe is 2.5 to 20 times more habitable today compared to when life first appeared on the Earth 4 billion years ago. We find that this increase in habitability will persist until the final stars die out over the next hundreds of billions of years.Comment: Under refereeing in Ap

    Deep sequencing approaches for the analysis of prokaryotic transcriptional boundaries and dynamics

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    The identification of the protein-coding regions of a genome is straightforward due to the universality of start and stop codons. However, the boundaries of the transcribed regions, conditional operon structures, non-coding RNAs and the dynamics of transcription, such as pausing of elongation, are non-trivial to identify, even in the comparatively simple genomes of prokaryotes. Traditional methods for the study of these areas, such as tiling arrays, are noisy, labour-intensive and lack the resolution required for densely-packed bacterial genomes. Recently, deep sequencing has become increasingly popular for the study of the transcriptome due to its lower costs, higher accuracy and single nucleotide resolution. These methods have revolutionised our understanding of prokaryotic transcriptional dynamics. Here, we review the deep sequencing and data analysis techniques that are available for the study of transcription in prokaryotes, and discuss the bioinformatic considerations of these analyses

    Misincorporation by RNA polymerase is a major source of transcription pausingin vivo

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    The transcription error rate estimated from mistakes in end product RNAs is 10−3–10−5. We analyzed the fidelity of nascent RNAs from all actively transcribing elongation complexes (ECs) in Escherichia coli and Saccharomyces cerevisiae and found that 1–3% of all ECs in wild-type cells, and 5–7% of all ECs in cells lacking proofreading factors are, in fact, misincorporated complexes. With the exception of a number of sequence-dependent hotspots, most misincorporations are distributed relatively randomly. Misincorporation at hotspots does not appear to be stimulated by pausing. Since misincorporation leads to a strong pause of transcription due to backtracking, our findings indicate that misincorporation could be a major source of transcriptional pausing and lead to conflicts with other RNA polymerases and replication in bacteria and eukaryotes. This observation implies that physical resolution of misincorporated complexes may be the main function of the proofreading factors Gre and TFIIS. Although misincorporation mechanisms between bacteria and eukaryotes appear to be conserved, the results suggest the existence of a bacteria-specific mechanism(s) for reducing misincorporation in protein-coding regions. The links between transcription fidelity, human disease, and phenotypic variability in genetically-identical cells can be explained by the accumulation of misincorporated complexes, rather than mistakes in mature RNA
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