RESUMO
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has affected millions worldwide since its outbreak in the winter of 2019. While extensive research has primarily focused on the deleterious respiratory effects of SARS-CoV-2 in recent years, its pan-tropism has become evident. Among the vital organs susceptible to SARS-CoV-2 infection is the kidney. Post SARS-CoV-2 infection, patients have developed coronavirus disease 19 (COVID-19), with reported incidences of COVID-19 patients developing acute kidney injury (AKI). Given COVID-19's multisystemic manifestation, our review focuses on the impact of SARS-CoV-2 infection within the renal system with an emphasis on the current hypotheses regarding the role of extracellular vesicles (EVs) in SARS-CoV-2 pathogenesis. Emerging studies have shown that SARS-CoV-2 can directly infect the kidney, whereas EVs are involved in the spreading of SARS-CoV-2 particles to other neighboring cells. Once the viral particles are within the kidney system, many proinflammatory signaling pathways are shown to be activated, resulting in AKI. Hence, clinical investigation of urinary proinflammatory components and total urinary extracellular vesicles (uEVs) with viral particles have been used to assess the severity of AKI in patients with COVID-19. Remarkedly, new emerging studies have shown the potential of mesenchymal stem cell-derived EVs (MSC-EVs) and ACE2-containing EVs as a hopeful therapeutic tool to inhibit SARS-CoV-2 RNA replication and block viral entry, respectively. Overall, understanding EVs' physiological role is crucial and hopefully will rejuvenate our therapeutic approach towards COVID-19 patients with AKI.
RESUMO
The ß-ketoacyl-[acyl carrier protein] synthase 1 (KASI) gene has been shown in model plant systems to be critical for the conversion of sucrose to oil. A previous study characterized the morphological and seed composition phenotypes associated with a reciprocal chromosomal translocation that disrupted one of the KASI genes in soybean. The principle findings of this work included a wrinkled seed phenotype, an increase in seed sucrose, a decrease in seed oil, and a low frequency of transmission of the translocation. However, it remained unclear which, if any, of these phenotypes were directly caused by the loss of KASI gene function, as opposed to the chromosomal translocation or other associated factors. In this study, CRISPR/Cas9 mutagenesis was used to generate multiple knockout alleles for this gene, and also one in-frame allele. These soybean plants were evaluated for morphology, seed composition traits, and genetic transmission. Our results indicate that the CRISPR/Cas9 mutants exhibited the same phenotypes as the chromosomal translocation mutant, validating that the observed phenotypes are caused by the loss of gene function. Furthermore, the plants harboring homozygous in-frame mutations exhibited similar phenotypes compared to the plants harboring homozygous knockout mutations. This result indicates that the amino acids lost in the in-frame mutant are essential for proper gene function. In-frame edits for this gene may need to target less essential and/or evolutionarily conserved domains in order to generate novel seed composition phenotypes.
