Cell Heterogeneity and Variability in Peripheral Nerve after Injury.

With the development of single-cell sequencing technology, the cellular composition of more and more tissues is being elucidated. As the whole nervous system has been extensively studied, the cellular composition of the peripheral nerve has gradually been revealed. By summarizing the current sequencing data, we compile the heterogeneities of cells that have been reported in the peripheral nerves, mainly the sciatic nerve. The cellular variability of Schwann cells, fibroblasts, immune cells, and endothelial cells during development and disease has been discussed in this review. The discovery of the architecture of peripheral nerves after injury benefits the understanding of cellular complexity in the nervous system, as well as the construction of tissue engineering nerves for nerve repair and axon regeneration.

Underlying Mechanisms of the Hedgehog-Like Panicle and Filamentous Leaf Tissue Symptoms Caused by Sclerospora graminicola in Foxtail Millet.

Downy mildew caused by Sclerospora graminicola is a systemic infectious disease affecting foxtail millet production in Africa and Asia. S. graminicola-infected leaves could be decomposed to a state where only the veins remain, resulting in a filamentous leaf tissue symptom. The aim of the present study was to investigate how S. graminicola influences the formation of the filamentous leaf tissue symptoms in hosts at the morphological and molecular levels. We discovered that vegetative hyphae expanded rapidly, with high biomass accumulated at the early stages of S. graminicola infection. In addition, S. graminicola could affect spikelet morphological development at the panicle branch differentiation stage to the pistil and stamen differentiation stage by interfering with hormones and nutrient metabolism in the host, resulting in hedgehog-like panicle symptoms. S. graminicola could acquire high amounts of nutrients from host tissues through secretion of ß-glucosidase, endoglucanase, and pectic enzyme, and destroyed host mesophyll cells by mechanical pressure caused by rapid expansion of hyphae. At the later stages, S. graminicola could rapidly complete sexual reproduction through tryptophan, fatty acid, starch, and sucrose metabolism and subsequently produce numerous oospores. Oospore proliferation and development further damage host leaves via mechanical pressure, resulting in a large number of degraded and extinct mesophyll cells and, subsequently, malformed leaves with only veins left, that is, "filamentous leaf tissue." Our study revealed the S. graminicola expansion characteristics from its asexual to sexual development stages, and the potential mechanisms via which the destructive effects of S. graminicola on hosts occur at different growth stages.

Pyrogallol promotes growth arrest by activating the p53-mediated up-regulation of p21 and p62/SQSTM1-dependent degradation of ß-catenin in nonsmall cell lung cancer cells.

Pyrogallol (1,2,3-trihydroxybenzene), a polyphenolic natural compound, has attracted considerable attention with regard to its potential anticancer activity. However, further study is needed to elucidate the underlying mechanism related to the antiNSCLC activity of pyrogallol and provide a comprehensive theoretical basis for better clinical utilization of pyrogallol. Our current study aims to investigate the effects and potential underlying mechanisms of pyrogallol on the inhibition of NSCLC growth. Our results showed that pyrogallol treatment induced cell cycle arrest at the G2/M phase and apoptosis in two different NSCLC cell lines. Mechanistically, we found that the induction of cell cycle arrest in NSCLC cells at the G2/M phase by pyrogallol was due to the upregulation of p21 in a p53-dependent manner. And blockade of p53 and p21 effectively abolished the cell cycle arrest at the G2/M phase. Meanwhile, p53 inhibition has been found to abrogate the pyrogallol-induced apoptosis of the two NSCLC cells. Moreover, we revealed that the inhibitory effects of pyrogallol on ß-catenin signaling resulted from autophagy initiation depending on p53 activation, accompanied by an increase in p62/SQSTM1 expression, thus p62 subsequently interacting with ubiquitinated ß-catenin and facilitating autophagic destruction of ß-catenin. Furthermore, in vivo experiments demonstrated that pyrogallol exerted growth inhibition on NSCLC with low toxicity through the same molecular mechanism as observed in vitro. Our findings could contribute to the understanding of the mechanism by which pyrogallol negatively regulates NSCLC growth, which could be effective in treating NSCLC.

Sclerospora graminicola Suppresses Plant Defense Responses by Disrupting Chlorophyll Biosynthesis and Photosynthesis in Foxtail Millet.

Downy mildew of foxtail millet is an important oomycete disease caused by Sclerospora graminicola, affecting the yield and quality of the crop. Foxtail millet infected with S. graminicola exhibit symptoms of leaf yellowing and leaf cracking. To uncover the pathogenic mechanism of this disease, we explored the effects on chlorophyll synthesis and photosynthesis of foxtail millet leaves infected by S. graminicola. An elite foxtail millet variety, JG21, susceptible to S. graminicola, was used as for this study. S. graminicola inhibited chlorophyll synthesis and caused loose mesophyll cell arrangement. In addition, some cells were severely vacuolated in S. graminicola-infected foxtail millet leaves at the early stages of infection. S. graminicola could invade the mesophyll cells through haustoria which destroyed the chloroplast structure at the middle stages of infection causing significant accumulation of osmiophilic particles (OPs) and disintegrated chloroplast grana lamellae. Furthermore, foxtail millet leaves split longitudinally at the later stages of infection. Chlorophyll and carotenoid contents in infected leaves decreased significantly compared with those in the control. Net photosynthetic rate (Pn) of leaves and stomatal conductance showed a downward trend, and intercellular carbon dioxide concentrations increased significantly following the infection with S. graminicola. A total of 1,618 differentially expressed genes (DEGs) were detected between the control group and the treatment groups using RNA sequencing (RNA-Seq) among S1-S5 stages. DEGs associated with "photosynthesis" and "light reaction" were enriched. Gene expression patterns showed that 91.3% of 23 genes related to chlorophyll synthesis and photosynthesis, were significantly down-regulated than the control during S1-S5 stages. Based on the gene expression dataset, weighed gene co-expression network analysis (WGCNA) with 19 gene co-expression modules related to photosynthesis revealed six hub genes related to chlorophyll synthesis, which were suppressed during infection. The results suggest that infection of S. graminicola led to weak chlorophyll synthesis and rapid chloroplasts disappearance in foxtail millet. The defense responses and resistance of foxtail millet to S. graminicola were inhibited because chloroplast structure and function were destroyed in leaves, and the sexual reproduction in S. graminicola could be completed rapidly.