Thylakoid grana stacking revealed by multiplex genome editing of LHCII encoding genes

Land plant chloroplasts differ from algal ones for their thylakoid membranes being organized in grana: piles of vesicles paired by their stromal surface, forming domains including Photosystem (PS) II and its antenna while excluding PS I and ATPase to stroma membranes, connecting grana stacks. The molecular basis of grana stacking remain unclear. We obtained genotypes lacking the trimeric antenna complex (Lhcb1-2-3), the monomeric Lhcb4-5-6, or both. Full deletion caused loss of grana, while either monomers or trimers support 50% stacking. The expression of Lhcb5 alone restored stacking at 50%, while Lhcb2 alone produced huge grana which broke down upon light exposure. Cyclic electron transport was maintained in the lack of stacking, while excitation energy balance between photosystems and the repair efficiency of damaged Photosystem II were affected. We conclude that grana evolved for need of regulating energy balance between photosystems under terrestrial canopy involving rapid changes in photon spectral distribution.

Intelligent systems for additive manufacturing-based repair in remanufacturing: a systematic review of its potential

The conventional component repair in remanufacturing involves human decision making that is influenced by several factors such as conditions of incoming cores, modes of failure, severity of damage, features and geometric complexities of cores and types of reparation required. Repair can be enhanced through automation using additive manufacturing (AM) technology. Advancements in AM have led to the development of directed energy deposition and laser cladding technology for repair of damaged parts and components. The objective of this systematic literature review is to ascertain how intelligent systems can be integrated into AM-based repair, through artificial intelligence (AI) approaches capable of supporting the nature and process of decision making during repair. The integration of intelligent systems in AM repair is expected to enhance resource utilization and repair efficiency during remanufacturing. Based on a systematic literature review of articles published during 2005–2021, the study analyses the activities of conventional repair in remanufacturing, trends in the applications of AM for repair using the current state-of-the-art technology and how AI has been deployed to facilitate repair. The study concludes with suggestions on research areas and opportunities that will further enhance the automation of component repair during remanufacturing using intelligent AM systems.

Evaluating the environmental maintenance impact (EMI): a carbon life cycle assessment (LCA) of the Singgora roof tiles repair in heritage buildings

PurposeHeritage buildings are consistently impacted by technical and pathological issues associated with their maintenance and conservation such as diminish of building's authenticity and damaging environmental impact. This paper aims to evaluate the environmental maintenance impact (EMI) of the Singgora roof tiles repair in heritage buildings. The EMI is an evaluation upon embodied carbon expenditure during maintenance phase, thus important in repair efficiency appraisal.Design/methodology/approachCalculation procedures within selected boundaries of life cycle assessment (LCA) and arbitrary period enabled evaluation of the EMI of Singgora roof tiles repair in heritage buildings during the maintenance phase.FindingsEvaluation of the EMI could be appreciated as a carbon LCA of Singgora roof tiles repair and has been recognised in embodied carbon expenditure reduction in the form of CO2 emissions mitigation. Importantly, the evaluation underpins decision-making for heritage buildings repair.Practical implicationsEMI evaluation encompasses all building types and forms, thus comprehends the associated applied methodologies. Moreover, the evaluation reflects the emerging environmental challenges of sustaining resilient buildings globally.Social implicationsEMI evaluation highlights options that may be adopted in repair. Indirectly, this implicates heritage building preservation and place's identity protection. Significantly, the evaluation supports environmentally focused conservation and promotes a sustainable repair approach.Originality/valueEMI evaluation of this paper may devoted to the holistic understanding of the complex relations between Singgora roof materials and their environmental performance. Meanwhile, the application of a carbon LCA had dictated integration of multidisciplinary of heritage buildings maintenance and conservation.

RPRM negatively regulates ATM levels involving its phosphorylation mediated by CDK4/CDK6

Sensitizing cancer cells to radio- and chemotherapy remains a hot topic in cancer treatment. Here it is identified that Protein Reprimo (RPRM) negatively regulates the levels of ataxia-telangiectasia mutated (ATM) protein kinase, a master regulator of DNA damage response (DDR) in the presence of DNA double-strand breaks (DSBs), resulting in impaired DNA repair efficiency and enhanced cellular sensitivity to genotoxic agents. Mechanistically, although RPRM is primarily located in cytoplasm, it rapidly translocates to nucleus shortly after induced by X-irradiation, interacts with ATM and promotes the nuclear export and proteasomal degradation of ATM. The nuclear translocation of RPRM is associated with its phosphorylation at serine 98, which is mediated by cyclin-dependent kinases 4/6 (CDK4/6). Inhibition of CDK4/6 stabilizes RPRM and promotes its nuclear import, in turn enhances the nuclear export of ATM and the reduction of ATM levels. As a result, RPRM overexpression and its phosphorylation inhibition sensitize cells to genotoxic agents. Moreover, RPRM deficiency significantly increases resistance to radiation-induced damage both in vitro and in vivo. These findings establish a crucial regulatory mechanism in which ATM is negatively modulated by RPRM, suggesting that RPRM may serve as a novel target for both cancer therapy and radiation protection.

Sequence Dependent Repair of 1,N6-Ethenoadenine by DNA Repair Enzymes ALKBH2, ALKBH3, and AlkB

Mutation patterns of DNA adducts, such as mutational spectra and signatures, are useful tools for diagnostic and prognostic purposes. Mutational spectra of carcinogens derive from three sources: adduct formation, replication bypass, and repair. Here, we consider the repair aspect of 1,N6-ethenoadenine (εA) by the 2-oxoglutarate/Fe(II)-dependent AlkB family enzymes. Specifically, we investigated εA repair across 16 possible sequence contexts (5′/3′ flanking base to εA varied as G/A/T/C). The results revealed that repair efficiency is altered according to sequence, enzyme, and strand context (ss- versus ds-DNA). The methods can be used to study other aspects of mutational spectra or other pathways of repair.

Strategies to Enhance the Resilience of an Urban Rail Transit Network

An urban rail transit (URT) system is an important component of an urban infrastructure system; however, it is vulnerable to disturbances, such as natural disasters and terrorist attacks. Constructing a highly resilient URT network has practical significance for enhancing its capability to respond to disturbances. In this paper, models are developed to optimize a URT network’s structure with regard to resilience and to enhance the resilience of a disrupted URT network. A bi-level programming model that aims to maximize a URT network’s global accessibility and global efficiency is formulated to optimize the structure of the network. A novel repair strategy, called the simulation repair strategy, is proposed to enhance the resilience of a disrupted URT network by optimizing the repair sequence of failed stations. The models are utilized to enhance the resilience of the Chengdu subway network. The result indicates that the bi-level programming model guides the construction of new links to optimize the structure of the Chengdu subway network. Deliberate attacks are more harmful to the Chengdu subway network than random attacks. The network’s operators need to pay attention to the operations of critical stations (e.g., Chunxi Road station and Tianfu Square station) to prevent disturbances from exerting considerable negative effects on the network’s normal operations. The simulation repair strategy exhibits higher repair efficiency than the conventional repair strategy, and it effectively enhances the resilience of the disrupted Chengdu subway network.

Comparative analyses of two primate species diverged by more than 60 million years show different rates but similar distribution of genome-wide UV repair events

Background Nucleotide excision repair is the primary DNA repair mechanism that removes bulky DNA adducts such as UV-induced pyrimidine dimers. Correspondingly, genome-wide mapping of nucleotide excision repair with eXcision Repair sequencing (XR-seq), provides comprehensive profiling of DNA damage repair. A number of XR-seq experiments at a variety of conditions for different damage types revealed heterogenous repair in the human genome. Although human repair profiles were extensively studied, how repair maps vary between primates is yet to be investigated. Here, we characterized the genome-wide UV-induced damage repair in gray mouse lemur, Microcebus murinus, in comparison to human. Results We derived fibroblast cell lines from mouse lemur, exposed them to UV irradiation, and analyzed the repair events genome-wide using the XR-seq protocol. Mouse lemur repair profiles were analyzed in comparison to the equivalent human fibroblast datasets. We found that overall UV sensitivity, repair efficiency, and transcription-coupled repair levels differ between the two primates. Despite this, comparative analysis of human and mouse lemur fibroblasts revealed that genome-wide repair profiles of the homologous regions are highly correlated, and this correlation is stronger for highly expressed genes. With the inclusion of an additional XR-seq sample derived from another human cell line in the analysis, we found that fibroblasts of the two primates repair UV-induced DNA lesions in a more similar pattern than two distinct human cell lines do. Conclusion Our results suggest that mouse lemurs and humans, and possibly primates in general, share a homologous repair mechanism as well as genomic variance distribution, albeit with their variable repair efficiency. This result also emphasizes the deep homologies of individual tissue types across the eukaryotic phylogeny.

Remediation of High Concentration Chromium Contaminated Soil by Enhanced Electrodynamic Method

High concentration of chromium salt has caused serious pollution to the environment since its production. The long-standing chromium residue has polluted the soil, and the total chromium concentration of some polluted soil has reached 30000 mg / kg. For the remediation of chromium contaminated soil, the enhanced electrodynamic method was proposed. In order to improve the efficiency of electrokinetic remediation of chromium contaminated soil, two enhanced electrokinetic remediation technologies were proposed: Electrokinetic oxidation enhanced remediation technology and electrokinetic enhanced remediation technology. (III) in soil was polluted by oxidant chromium oxide to increase the content of dissolved (VI),so as to improve the efficiency of electric repair, in order to find a suitable PRB medium as a breakthrough to improve the repair efficiency. The experimental results show that compared with the traditional electrodynamic technology, the enhanced electrodynamic method can effectively improve the removal rate of total chromium in the soil, and provide technical support for the enhanced electrodynamic remediation of chromium contaminated soil. The pH control system makes the pH of anode and cathode electrolyte always maintain acidic, and the H+ migration speed is faster than that of OH-, and the pH of soil near the anode is lower than that near the cathode.

Actin-Related Protein 6 (Arp6) Influences Double-Strand Break Repair in Yeast

DNA double-strand breaks (DSBs) are the most deleterious form of DNA damage and are repaired through non-homologous end-joining (NHEJ) or homologous recombination (HR). Repair initiation, regulation and communication with signaling pathways require several histone-modifying and chromatin-remodeling complexes. In budding yeast, this involves three primary complexes: INO80-C, which is primarily associated with HR, SWR1-C, which promotes NHEJ, and RSC-C, which is involved in both pathways as well as the general DNA damage response. Here we identify ARP6 as a factor involved in DSB repair through an RSC-C-related pathway. The loss of ARP6 significantly reduces the NHEJ repair efficiency of linearized plasmids with cohesive ends, impairs the repair of chromosomal breaks, and sensitizes cells to DNA-damaging agents. Genetic interaction analysis indicates that ARP6, MRE11 and RSC-C function within the same pathway, and the overexpression of ARP6 rescues rsc2∆ and mre11∆ sensitivity to DNA-damaging agents. Double mutants of ARP6, and members of the INO80 and SWR1 complexes, cause a significant reduction in repair efficiency, suggesting that ARP6 functions independently of SWR1-C and INO80-C. These findings support a novel role for ARP6 in DSB repair that is independent of the SWR1 chromatin remodeling complex, through an apparent RSC-C and MRE11-associated DNA repair pathway.