The inhibitory effect of extracellular DNA (exDNA) on the growth of conspecific individuals was demonstrated in different kingdoms. In plants, the inhibition has been observed on root growth and seed germination, demonstrating its role in plant–soil negative feedback. Several hypotheses have been proposed to explain the early response to exDNA and the inhibitory effect of conspecific exDNA. We here contribute with a whole-plant transcriptome profiling in the model species Arabidopsis thaliana exposed to extracellular self- (conspecific) and nonself- (heterologous) DNA. The results highlight that cells distinguish self- from nonself-DNA. Moreover, confocal microscopy analyses reveal that nonself-DNA enters root tissues and cells, while self-DNA remains outside. Specifically, exposure to self-DNA limits cell permeability, affecting chloroplast functioning and reactive oxygen species (ROS) production, eventually causing cell cycle arrest, consistently with macroscopic observations of root apex necrosis, increased root hair density and leaf chlorosis. In contrast, nonself-DNA enters the cells triggering the activation of a hypersensitive response and evolving into systemic acquired resistance. Complex and different cascades of events emerge from exposure to extracellular self- or nonself-DNA and are discussed in the context of Damage- and Pathogen-Associated Molecular Patterns (DAMP and PAMP, respectively) responses.

The capacity to actively release genetic material into the extracellular environment has been reported for bacteria, archaea, fungi, and in general, for microbial communities, but it is also described in the context of multicellular organisms, animals and plants. This material is often present in matrices that locate outside the cells. Extracellular matrices have important roles in defense response and disease in microbes, animal and plants cells, appearing as barrier against pathogen invasion or for their recognition. Specifically, neutrophils extracellular traps (NETs) in animals and root extracellular traps (RETs) in plants, are recognized to be important players in immunity. A growing amount of evidence revealed that the extracellular DNA, in these contexts, plays an active role in the defense action. Moreover, the protective role of extracellular DNA against antimicrobials and mechanical stress also appears to be confirmed in bacterial biofilms. In parallel, recent efforts highlighted different roles of self (homologous) and non-self (heterologous) extracellular DNA, paving the way to discussions on its role as a “Damage-associated molecular pattern” (DAMP). We here provide an evolutionary overview on extracellular DNA in extracellular matrices like RETs, NETs, and microbial biofilms, discussing on its roles and inferring on possible novel functionalities.

Glutathione-S-transferases (GSTs) are encoded by genes belonging to a wide ubiquitous family in aerobic species and catalyze the conjugation of electrophilic substrates to glutathione (GSH). GSTs are divided in different classes, both in plants and animals. In plants, GSTs function in several pathways, including those related to secondary metabolites biosynthesis, hormone homeostasis, defense from pathogens and allow the prevention and detoxification of damage from heavy metals and herbicides. 1107 GST protein sequences from 20 different plant species with sequenced genomes were analyzed. Our analysis assigns 666 unclassified GSTs proteins to specific classes, remarking the wide heterogeneity of this gene family. Moreover, we highlighted the presence of further subclasses within each class. Regarding the class GST-Tau, one possible subclass appears to be present in all the Tau members of ancestor plant species. Moreover, the results highlight the presence of members of the Tau class in Marchantiophytes and confirm previous observations on the absence of GST-Tau in Bryophytes and green algae. These results support the hypothesis regarding the paraphyletic origin of Bryophytes, but also suggest that Marchantiophytes may be on the same branch leading to superior plants, depicting an alternative model for green plants evolution.

The main hallmarks of cancer diseases are the evasion of programmed cell death, uncontrolled cell division, and the ability to invade adjacent tissues. The explosion of omics technologies offers challenging opportunities to identify molecular agents and processes that may play relevant roles in cancer. They can support comparative investigations, in one or multiple experiments, exploiting evidence from one or multiple species. Here, we analyzed gene expression data from induction of programmed cell death and stress response in Homo sapiens and compared the results with Saccharomyces cerevisiae gene expression during the response to cell death. The aim was to identify conserved candidate genes associated with Homo sapiens cell death, favored by crosslinks based on orthology relationships between the two species. We identified differentially-expressed genes, pathways that are significantly dysregulated across treatments, and characterized genes among those involved in induced cell death. We investigated on co-expression patterns and identified novel genes that were not expected to be associated with death pathways, that have a conserved pattern of expression between the two species. Finally, we analyzed the resulting list by HumanNet and identified new genes predicted to be involved in cancer. The data integration and the comparative approach between distantly-related reference species that were here exploited pave the way to novel discoveries in cancer therapy and also contribute to detect conserved genes potentially involved in programmed cell death.

It is today widely accepted that a healthy diet is very useful to prevent the risk for cancer or its deleterious effects. Nutrigenomics studies are therefore taking place with the aim to test the effects of nutrients at molecular level and contribute to the search for anti-cancer treatments. These efforts are expanding the precious source of information necessary for the selection of natural compounds useful for the design of novel drugs or functional foods. Here we present a computational study to select new candidate compounds that could play a role in cancer prevention and care. Starting from a dataset of genes that are co-expressed in programmed cell death experiments, we investigated on nutrigenomics treatments inducing apoptosis, and searched for compounds that determine the same expression pattern. Subsequently, we selected cancer types where the genes showed an opposite expression pattern and we confirmed that the apoptotic/nutrigenomics expression trend had a significant positive survival in cancer-affected patients. Furthermore, we considered the functional interactors of the genes as defined by public protein-protein interaction data, and inferred on their involvement in cancers and/or in programmed cell death. We identified 7 genes and, from available nutrigenomics experiments, 6 compounds effective on their expression. These 6 compounds were exploited to identify, by ligand-based virtual screening, additional molecules with similar structure. We checked for ADME criteria and selected 23 natural compounds representing suitable candidates for further testing their efficacy in apoptosis induction. Due to their presence in natural resources, novel drugs and/or the design of functional foods are conceivable from the presented results.

Background . A novel coronavirus, the SARS-CoV2, was revealed to be the cause of COVID19, the pandemic disease that already provoked more than 555.324 deaths in the world (July 10, 2020). No vaccine treatment has been defined against SARS-CoV2 or other human coronaviruses (HCoVs), including those causing epidemic infections, neither appropriate strategies for prevention and care are yet officially suggested. Scope and approach . We reviewed scientific literature on natural compounds that were defined as potentially effective against human coronaviruses. Our desk research identified non-chemically modified natural compounds that were shown (in vitro) and/or predicted (in silico) to act against one or more phases of human coronaviruses cell cycle. We selected all available information, merged and annotated the data to define a comprehensive list of natural compounds, describing their chemical classification, the source, the action, the specific target in the viral infection. Our aim was to collect possible compounds for prevention and care against human coronaviruses. Key findings and conclusions . The definition of appropriate interventions against viral diseases need a comprehensive view on the infection dynamics and on necessary treatments. Viral targeting compounds to be exploited in food sciences could be of relevant interest to this aim. We collected 174 natural compounds showing effects against human infecting coronaviruses, providing a curated annotation on actions and targets. The data are available in anti-HCoV , a web accessible resource to be exploited for testing and in vivo trials. The website is here launched to favour a community based cooperative effort to call for contribution and expand the collection. To be ready to fight.

No abstract

Programmed cell death involves complex molecular pathways in both eukaryotes and prokaryotes. In Escherichia coli, the toxin–antitoxin system (TA-system) has been described as a programmed cell death pathway in which mRNA and ribosome organizations are modified, favoring the production of specific death-related proteins, but also of a minor portion of survival proteins, determining the destiny of the cell population. In the eukaryote Saccharomyces cerevisiae, the ribosome was shown to change its stoichiometry in terms of ribosomal protein content during stress response, affecting the relative proportion between ohnologs, i.e., the couple of paralogs derived by a whole genome duplication event. Here, we confirm the differential expression of ribosomal proteins in yeast also during programmed cell death induced by acetic acid, and we highlight that also in this case pairs of ohnologs are involved. We also show that there are different trends in cytosolic and mitochondrial ribosomal proteins gene expression during the process. Moreover, we show that the exposure to acetic acid induces the differential expression of further genes coding for products related to translation processes and to rRNA post-transcriptional maturation, involving mRNA decapping, affecting translation accuracy, and snoRNA synthesis. Our results suggest that the reprogramming of the overall translation apparatus, including the cytosolic ribosome reorganization, are relevant events in yeast programmed cell death induced by acetic acid.