First report in China of Fusarium humuli as a causative agent of Chinese yam wilt.

Wilt is one the most serious soil-born fungal diseases of Chinese yam (Dioscorea polystachya Turczaninow cv. Tiegun), affecting plant production in many growing regions in Jiangxi province, China. The average annual incidence of wilt is 45-80%. In 2020, affected plants with wilt symptoms including withered and dried leaves, vascular discoloration, and brown necrotic stem lesions at the soil line or in the crown of the plant (Figure 1A-D) were collected from the Ruichang, Yongfeng and Taihe production areas (four fields per location) in Jiangxi province. A total of fifteen isolates were recovered from the infected stem tissues of Chinese yam and purified by single spore cultures on PDA growth medium. The fifteen isolates were similar in morphology so isolate JXRC11 was selected to be representative of the group. Pure fungal colonies of JXRC11were found to be round, white, with margin entire (Figure 1E). Macroconidia with 3-5 septations were straight to slightly curved, 23.8-40.3 µm in length and 2.6-3.9 µm in width, with predominantly 5-septate macroconidia on carnation leaf agar (CLA) (Figure 1F). However, neither microconidia or chlamydospores were observed on CLA. The morphological characteristics of the isolate were consistent with the description observed previously for Fusarium humuli species complex (Wang et al. 2019). To confirm morphological identification, ITS, CAM, TEF-1α, RPB1 and RPB2 were amplified using the primers ITS5/ITS4 (White et al. 1990), CL1/CL2A (O'Donnell et al. 2000), EF1/EF2 (O'Donnell et al. 1998), Fa/G2R (O'Donnell et al. 2010), and 5f2/11ar (O'Donnell et al. 2010), respectively. BLASTn analysis of the ITS sequence (GenBank accession no. MZ768912), EF-1α (MZ824669), CAM (MZ824670), RPB1 (MZ824672) and RPB2 (MZ824673) alignment showed 99.55%, 99.68%, 99.85%, 97.61% and 99.76% identity to those of F. humuli CQ1039 (MK280845, MK289570, MK289712, MK289840 and MK289724), respectively. Multilocus phylogenetic analyses showed that the sequences of ITS, CAM, EF-1α, RPB1, and RPB2 of the isolate belonged to the incarnatum clade (FIESC-33) of the F. incarnatum-equiseti species complex with an independent branch (Figure 2). Pathogenicity tests were conducted on one-month-old Chinese yam seedlings using a seedling root dip method (Li et al. 2013). The roots and rhizomes of seedlings grown to two meters in height were dipped into spore suspensions (1×106 spores/mL) of isolate JXRC11 for 30 min and then transferred into 20 cm diameter plastic pots containing steam-sterilized soil and placed in a greenhouse under 12 h photoperiod. After 15 d, the inoculated seedlings showed typical wilt symptoms similar to those observed in farm fields, whereas the control remained unaffected (Figure 1G-H). The pathogen was then re-isolated from the infected plants, the re-isolations were identified as F. humuli by sequencing EF-1α, fulfilling the Koch's postulates. It has been reported that the pathogen F. oxysporum Schlecht causes Fusarium wilt in five species of Dioscorea (Nwankiti and Arene, 1978). Moreover, at least 5 species of Fusarium were identified as a causative agent of Chinese yam wilt (Fang et al. 2020). To our knowledge, this is the first report of Fusarium wilt disease on Chinese yam caused by a member of the F. humuli in Jiangxi, China. This report will contribute to developing management strategies to control the disease.

Complete genome sequence of the sesame pathogen Ralstonia solanacearum strain SEPPX 05.

Ralstonia solanacearum is a soil-borne phytopathogen associated with bacterial wilt disease of sesame. R. solanacearum is the predominant agent causing damping-off from tropical to temperate regions. Because bacterial wilt has decreased the sesame industry yield, we sequenced the SEPPX05 genome using PacBio and Illumina HiSeq 2500 systems and revealed that R. solanacearum strain SEPPX05 carries a bipartite genome consisting of a 3,930,849 bp chromosome and a 2,066,085 bp megaplasmid with 66.84% G+C content that harbors 5,427 coding sequences. Based on the whole genome, phylogenetic analysis showed that strain SEPPX05 is grouped with two phylotype I strains (EP1 and GMI1000). Pan-genomic analysis shows that R. solanacearum is a complex species with high biological diversity and was able to colonize various environments during evolution. Despite deletions, insertions, and inversions, most genes of strain SEPPX05 have relatively high levels of synteny compared with strain GMI1000. We identified 104 genes involved in virulence-related factors in the SEPPX05 genome and eight absent genes encoding T3Es of GMI1000. Comparing SEPPX05 with other species, we found highly conserved secretion systems central to modulating interactions of host bacteria. These data may provide important clues for understanding underlying pathogenic mechanisms of R. solanacearum and help in the control of sesame bacterial wilt.

Apolipoprotein E-Mimetic Peptide COG1410 Promotes Autophagy by Phosphorylating GSK-3ß in Early Brain Injury Following Experimental Subarachnoid Hemorrhage.

COG1410, a mimetic peptide derived from the apolipoprotein E (apoE) receptor binding region, exerts positive effect on neurological deficits in early brain injury (EBI) after experimental subarachnoid hemorrhage (SAH). Currently the neuroprotective effect of COG1410 includes inhibiting BBB disruption, reducing neuronal apoptosis, and neuroinflammation. However, the effect and mechanism of COG1410 to subcellular organelles disorder have not been fully investigated. As the main pathway for recycling long-lived proteins and damaged organelles, neuronal autophagy is activated in SAH and exhibits neuroprotective effects by reducing the insults of EBI. Pharmacologically elevated autophagy usually contributes to alleviated brain injury, while few of the agents achieved clinical transformation. In this study, we explored the activation of autophagy during EBI by measuring the Beclin-1 and LC3B-II protein levels. Administration of COG1410 notably elevated the autophagic markers expression in neurons, simultaneously reversed the neurological deficits. Furthermore, the up-regulated autophagy by COG1410 was further promoted by p-GSK-3ß agonist, whereas decreased by p-GSK-3ß inhibitor. Taken together, these data suggest that the COG1410 might be a promising therapeutic strategy for EBI via promoting autophagy in SAH.

Peli1 Contributions in Microglial Activation, Neuroinflammatory Responses and Neurological Deficits Following Experimental Subarachnoid Hemorrhage.

Early brain injury (EBI) following subarachnoid hemorrhage (SAH) is closely associated with neuroinflammation. Microglial activation is an early event that leads to neuroinflammation after SAH. Peli1 is an E3 ubiquitin ligase that mediates the induction of pro-inflammatory cytokines in microglia. Here we report Peli1 contributions in SAH mediated brain pathology. An SAH model was induced by endovascular perforation in adult male C57BL/6J mice. Peli1 was markedly induced in mice brains in a time-dependent manner and was predominantly expressed in CD16/32-positive microglia after SAH. Using genetic approaches, we demonstrated that decreased Peli1 significantly improved neurological deficits, attenuated brain edema, reduced over-expression of pro-inflammatory cytokine IL-6 and modified apoptotic/antiapoptotic biomarkers. In addition, Peli1 downregulation suppressed ERK and JNK phosphorylation levels via the downregulation of cIAP1/2 expression, subsequently reducing inducible nitric oxide synthase (iNOS) expression after SAH. Therefore, these findings demonstrate that Peli1 contributes to microglia-mediated neuroinflammation in EBI by mediating cIAP1/2 activation, thus promoting the activation of MyD88-dependent MAPK pathway after experimental SAH. Our findings also showed that Peli1 could promote the expression of M1 microglia polarization biomarker CD16/32 and iNOS after SAH. Targeting Peli1 exerts neuroprotective effects during EBI after SAH, thus could provide potential option for prevention-therapy in high-risk individuals.

High-Throughput Sequencing and Co-Expression Network Analysis of lncRNAs and mRNAs in Early Brain Injury Following Experimental Subarachnoid Haemorrhage.

Subarachnoid haemorrhage (SAH) is a fatal neurovascular disease following cerebral aneurysm rupture with high morbidity and mortality rates. Long non-coding RNAs (lncRNAs) are a type of mammalian genome transcript, are abundantly expressed in the brain and are involved in many nervous system diseases. However, little is currently known regarding the influence of lncRNAs in early brain injury (EBI) after SAH. This study analysed the expression profiles of lncRNAs and mRNAs in SAH brain tissues of mice using high-throughput sequencing. The results showed a remarkable difference in lncRNA and mRNA transcripts between SAH and control brains. Approximately 617 lncRNA transcripts and 441 mRNA transcripts were aberrantly expressed at 24 hours after SAH. Gene ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis indicated that the differentially expressed mRNAs were mostly involved in inflammation. Based on the lncRNA/mRNA co-expression network, knockdown of fantom3_F730004F19 reduced the mRNA and protein levels of CD14 and toll-like receptor 4 (TLR4) and attenuated inflammation in BV-2 microglia cells. These results indicate that lncRNA fantom3_F730004F19 may be associated with microglia induced inflammation via the TLR signaling pathway in EBI following SAH. LncRNA represent a potential therapeutic target for the prognosis, diagnosis, and treatment of SAH.

RNA silencing suppressor Pns11 of rice gall dwarf virus induces virus-like symptoms in transgenic rice.

Transgenic rice (Oryza sativa) plants expressing the Pns11 protein of rice gall dwarf virus (RGDV) displayed multiple abnormal phenotypes, some of which were highly reminiscent of the symptoms observed in RGDV-infected rice. Further analysis indicated that the apparent alterations in plant growth and morphology were correlated with the expression levels of microRNA160, microRNA162, microRNA167, microRNA168, and the microRNA target OsARF8. Especially, the striking dwarfing phenotype depended on the high expression level of microRNA167. By analogy to other categories of plant viruses, the RNA silencing suppressors encoded by plant dsRNA viruses function as pathogenicity determinants. These findings significantly deepen our current mechanistic understanding of the RNA silencing suppressor (VSR) encoded by a dsRNA virus and provide additional evidence that interference with microRNA expression is a VSR function utilized by a diverse range of viruses.