Physical conditions in QSO absorbers from fine-structure absorption lines

We calculate theoretical population ratios of the ground fine-structure levels of some atoms/ions which typically exhibit UV lines in the spectra of QSO absorbers redward the Ly-alpha forest: C0, C+, O0, Si+ and Fe+. The most reliable atomic data available is employed and a variety of excitation mechanisms considered: collisions with several particles in the medium, direct excitation by photons from the cosmic microwave background radiation (CMBR) and fluorescence induced by a UV field present. The theoretical population ratios are confronted with the corresponding column density ratios of C I and C II lines observed in damped Ly-alpha (DLA) and Lyman Limit (LL) systems collected in the recent literature to infer their physical conditions. The volumetric density of neutral hydrogen in DLA systems is constrained to be lower than tens of cm^-3 (or a few cm^-3 in the best cases) and the UV radiation field intensity must be lower than two orders of magnitude the radiation field of the Galaxy (one order of magnitude in the best cases). Their characteristic sizes are higher than a few pc (tens of pc in the best cases) and lower limits for their total masses vary from 10^0 to 10^5 solar masses. For the only LL system in our sample, the electronic density is constrained to be n_e<0.15 cm^-3. We suggest that the fine-structure lines may be used to discriminate between the current accepted picture of the UV extragalatic background as the source of ionization in these systems against a local origin for the ionizing radiation as supported by some authors. We also investigate the validity of the temperature-redshift relation of the CMBR predicted by the standard model and study the case for alternative models.Comment: 16 pages, 12 figure

Metabolite profiling at the cellular and subcellular level reveals metabolites associated with salinity tolerance in sugar beet

Hossain MS, Persicke M, ElSayed AI, Kalinowski J, Dietz K-J. Metabolite profiling at the cellular and subcellular level reveals metabolites associated with salinity tolerance in sugar beet. Journal of Experimental Botany. 2017;68(21-22):5961-5976.Sugar beet is among the most salt-tolerant crops. This study aimed to investigate the metabolic adaptation of sugar beet to salt stress at the cellular and subcellular levels. Seedlings were grown hydroponically and subjected to stepwise increases in salt stress up to 300 mM NaCl. Highly enriched fractions of chloroplasts were obtained by nonaqueous fractionation using organic solvents. Total leaf metabolites and metabolites in chloroplasts were profiled at 3 h and 14 d after reaching the maximum salinity stress of 300 mM NaCl. Metabolite profiling by gas chromatography- mass spectrometry (GC-MS) resulted in the identification of a total of 83 metabolites in leaves and chloroplasts under control and stress conditions. There was a lower abundance of Calvin cycle metabolites under salinity whereas there was a higher abundance of oxidative pentose phosphate cycle metabolites such as 6-phosphogluconate. Accumulation of ribose-5-phosphate and ribulose-5-phosphate coincided with limitation of carbon fixation by ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco). Increases in glycolate and serine levels indicated that photorespiratory metabolism was stimulated in salt-stressed sugar beet. Compatible solutes such as proline, mannitol, and putrescine accumulated mostly outside the chloroplasts. Within the chloroplast, putrescine had the highest relative level and probably assisted in the acclimation of sugar beet to high salinity stress. The results provide new information on the contribution of chloroplasts and the extra-chloroplast space to salinity tolerance via metabolic adjustment in sugar beet

PrimPol-dependent single-stranded gap formation mediates homologous recombination at bulky DNA adducts

Stalled replication forks can be restarted and repaired by RAD51-mediated homologous recombination (HR), but HR can also perform post-replicative repair after bypass of the obstacle. Bulky DNA adducts are important replication-blocking lesions, but it is unknown whether they activate HR at stalled forks or behind ongoing forks. Using mainly BPDE-DNA adducts as model lesions, we show that HR induced by bulky adducts in mammalian cells predominantly occurs at post-replicative gaps formed by the DNA/RNA primase PrimPol. RAD51 recruitment under these conditions does not result from fork stalling, but rather occurs at gaps formed by PrimPol re-priming and resection by MRE11 and EXO1. In contrast, RAD51 loading at double-strand breaks does not require PrimPol. At bulky adducts, PrimPol promotes sister chromatid exchange and genetic recombination. Our data support that HR at bulky adducts in mammalian cells involves post-replicative gap repair and define a role for PrimPol in HR-mediated DNA damage tolerance

Repriming DNA synthesis: an intrinsic restart pathway that maintains efficient genome replication

To bypass a diverse range of fork stalling impediments encountered during genome replication, cells possess a variety of DNA damage tolerance (DDT) mechanisms including translesion synthesis, template switching, and fork reversal. These pathways function to bypass obstacles and allow efficient DNA synthesis to be maintained. In addition, lagging strand obstacles can also be circumvented by downstream priming during Okazaki fragment generation, leaving gaps to be filled post-replication. Whether repriming occurs on the leading strand has been intensely debated over the past half-century. Early studies indicated that both DNA strands were synthesised discontinuously. Although later studies suggested that leading strand synthesis was continuous, leading to the preferred semi-discontinuous replication model. However, more recently it has been established that replicative primases can perform leading strand repriming in prokaryotes. An analogous fork restart mechanism has also been identified in most eukaryotes, which possess a specialist primase called PrimPol that conducts repriming downstream of stalling lesions and structures. PrimPol also plays a more general role in maintaining efficient fork progression. Here, we review and discuss the historical evidence and recent discoveries that substantiate repriming as an intrinsic replication restart pathway for maintaining efficient genome duplication across all domains of life