ABSTRACT
Tissue-specific implications of SARS-CoV-2-encoded accessory proteins are not fully understood. SARS-CoV-2 infection can severely affect three major organs-the heart, lungs, and brain. We analyzed SARS-CoV-2 ORF3a interacting host proteins in these three major organs. Furthermore, we identified common and unique interacting host proteins and their targeting miRNAs (lung and brain) and delineated associated biological processes by reanalyzing RNA-seq data from the brain (COVID-19-infected/uninfected choroid plexus organoid study), lung tissue from COVID-19 patients/healthy subjects, and cardiomyocyte cells-based transcriptomics analyses. Our in silico studies showed ORF3a interacting proteins could vary depending upon tissues. The number of unique ORF3a interacting proteins in the brain, lungs, and heart were 10, 7, and 1, respectively. Though common pathways influenced by SARS-CoV-2 infection were more, unique 21 brain and 7 heart pathways were found. One unique pathway for the heart was negative regulation of calcium ion transport. Reported observations of COVID-19 patients with a history of hypertension taking calcium channel blockers (CCBs) or dihydropyridine CCBs had an elevated rate of intubation or increased rate of intubation/death, respectively. Also, the likelihood of hospitalization of chronic CCB users with COVID-19 was greater in comparison to long-term angiotensin-converting enzyme inhibitors/angiotensin receptor blockers users. Further studies are necessary to confirm this. miRNA analysis of ORF3a interacting proteins in the brain and lungs revealed 3 of 37 brain miRNAs and 1 of 25 lung miRNAs with high degree and betweenness indicating their significance as hubs in the interaction network. Our study could help in identifying potential tissue-specific COVID-19 drug/drug repurposing targets.
ABSTRACT
Changes in environmental conditions like temperature and light critically influence crop production. To deal with these changes, plants possess various photoreceptors such as Phototropin (PHOT), Phytochrome (PHY), Cryptochrome (CRY), and UVR8 that work synergistically as sensor and stress sensing receptors to different external cues. PHOTs are capable of regulating several functions like growth and development, chloroplast relocation, thermomorphogenesis, metabolite accumulation, stomatal opening, and phototropism in plants. PHOT plays a pivotal role in overcoming the damage caused by excess light and other environmental stresses (heat, cold, and salinity) and biotic stress. The crosstalk between photoreceptors and phytohormones contributes to plant growth, seed germination, photo-protection, flowering, phototropism, and stomatal opening. Molecular genetic studies using gene targeting and synthetic biology approaches have revealed the potential role of different photoreceptor genes in the manipulation of various beneficial agronomic traits. Overexpression of PHOT2 in Fragaria ananassa leads to the increase in anthocyanin content in its leaves and fruits. Artificial illumination with blue light alone and in combination with red light influence the growth, yield, and secondary metabolite production in many plants, while in algal species, it affects growth, chlorophyll content, lipid production and also increases its bioremediation efficiency. Artificial illumination alters the morphological, developmental, and physiological characteristics of agronomic crops and algal species. This review focuses on PHOT modulated signalosome and artificial illumination-based photo-biotechnological approaches for the development of climate-smart crops.
ABSTRACT
Acid evokes pain by exciting nociceptors; the acid sensors are proton-gated ion channels that depolarize neurons. The naked mole-rat (Heterocephalus glaber) is exceptional in its acid insensitivity, but acid sensors (acid-sensing ion channels and the transient receptor potential vanilloid-1 ion channel) in naked mole-rat nociceptors are similar to those in other vertebrates. Acid inhibition of voltage-gated sodium currents is more profound in naked mole-rat nociceptors than in mouse nociceptors, however, which effectively prevents acid-induced action potential initiation. We describe a species-specific variant of the nociceptor sodium channel Na(V)1.7, which is potently blocked by protons and can account for acid insensitivity in this species. Thus, evolutionary pressure has selected for an Na(V)1.7 gene variant that tips the balance from proton-induced excitation to inhibition of action potential initiation to abolish acid nociception.