Key genes needed for maintenance and growth for the two pathogens, Fusarium graminearum and Magnaporthe oryzae, were identified. These are genes that are induced in response to maintenance requirements (stress) and growth requirements. The processes involved are synthesizing arginine, synthesis of DNA-bases, nitric oxide synthesis needing arginine, autophagy, DNA synthesis, and DNA repair. A simplified regulatory network for these key genes for both organisms was constructed as a hypothesis for the work, and procedures previously developed to use sets of downloaded transcriptomic data were used to test hypotheses concerning what time under the course of infection of plants the key genes are expressed. The analysis shows that the transcription efforts (costs) to maintain the fungal cells (maintenance) are high before infection and during early infection. During the following biotrophic stage, maintenance activities drop, followed by a dramatic increase in the necrotrophic stage transition. Finally, in the necrotrophic stage, maintenance is again lower despite the high growth rate that can also cause stress. All identified genes' expressions behaved almost similar with an increased expression in the biotrophy-necrotrophy transition for both fungi except the DNA repair genes PARP/PARG that was not responding or absent (PARG) in the mainly clonal M. oryzae. This PARG expression pattern might indicate that M. oryzae is more subject to evolution by point mutations than F. graminearum, where sexual reproduction is frequent. The potential consequences of this in the development and the accelerated breakage of host species resistance in a Red Queen dynamics scenario are discussed. The analysis demonstrates the possibility of using large transcriptome datasets and co-regulations between key genes to test hypotheses. This technique's advantages complement molecular techniques that employ knockouts and over-expression of target genes to suggest that genes' roles are discussed.

The emerging new Coronaviridae member, nCoV 19, outbreak announced a pandemic by WHO with an increased morbidity and mortality rate worldwide. nCoV 19 known as the third highly pathogen coronavirus in the human population after the severe acute respiratory syndrome coronavirus (SARS-CoV) and the Middle East respiratory syndrome coronavirus (MERS-CoV), the nCoV 19. The renin-angiotensin (RAS) signaling pathway, oxidative stress and cell death, cytokines storm and endothelial dysfunction are four major pathways involved in the pathogenesis of nCoV 19. Acute respiratory distress syndrome (ARDS) generally develops with a massive oxidative/nitrosative stress following virus entry and RAS activation. The DNA damage subsequent to oxidative burst activates poly-ADP ribose polymerase-1 (PARP-1), viral macrodomain (NSP3) poly (ADP-ribose) glycohydrolase (PARG) and transient receptor potential channel, melastatin 2 (TRPM2) in a sequential manner ultimately leading to apoptosis and necrosis due to NAD and ATP depletion. Regarding the molecular mechanisms involved in nCoV 19 pathogenesis, angiotensin II receptor blockers and/or PARP, PARG and TRPM2 blockers could be engaged as therapeutic candidates for inhibition of RAS and quenching oxidative stress, respectively. In this review, the molecular aspects of nCoV 19 pathogenesis would be studied precisely and possible therapeutic targets would be proposed. It is recommended to evaluate the proposed drugs and supplements via registered clinical trials along with conventional guideline-based multi-drug regimen.

Among post-translational modifications of proteins, ADP-ribosylation has been studied for over fifty years, assigning to this PTM a large set of functions, including DNA repair, transcription and cell signaling. This review presents an update on the function of a large set of enzyme writers, the readers that are recruited by the modified targets, and the erasers that reverse the modification to the original amino acid residue, removing the covalent bonds formed. In particular, the review provides details on the involvement of the enzymes performing MAR/PAR cycling in cancers. Of note, there is potential for application of the inhibitors developed for cancer also in the therapy of non-oncological diseases such as the protection against oxidative stress, suppression of inflammatory responses, and the treatment of neurodegenerative diseases. This field of studies is not concluded, since novel enzymes are being discovered at a rapid pace.