Li, D. D. | Search bioRxiv

bioRxiv2023

Hierarchical Clustering and Omics Analysis Revealed Massive Molecular Shifts in a Tree under Combined Hypoxia and Salinity

Field and Greenhouse studies that attempted to describe the molecular responses of trees under waterlogging (WL) combined with salinity (ST) are quasi-inexistent. To dissect plant-specific molecular responses and patterns under SWL, we integrated transcriptional and metabolic analyses involving common differentially expressed genes (DEGs) and metabolites (DMs) patterns in Dalbergia odorifera leaflets. SWL-treated seedlings exhibited an impressively high number of DEGs and DMs compared to ST or WL. Although the main common DEGs and DMs showed a neutral pattern, gene ontology enrichment following the classification in different functional categories of SWL-transcripts displayed a predominant synergistic pattern mode. Hierarchical and silhouette analysis regrouped different morpho-physiological clusters following the treatment, SWL was mainly grouped with both single stress. SWL induced a massive shutdown of the photosynthesis apparatus through LHCBs- and PSA-related genes. Starch and plastoglobuli synthesis appeared to be drastically affected by SWL, while ABA content confirmed by ABA synthesis related-genes (ABF, ABA1 and NCED) variations showed a less-needed role. NXN (Nucleoredoxin) genes are the main factors that sustain the antioxidant system under SWL. Here we provide the first molecular responses, characterization and patterns of a tree under SWL that would significantly shed light on our understanding of the molecular mechanisms underlying combined stress.

plant biology↗

bioRxiv2019

E-cadherin binds glycosylated sodium-taurocholate cotransporting polypeptide to facilitate hepatitis B virus entry

Hepatitis B virus (HBV) continues to pose a serious public health risk and is one of the major causes of chronic liver disease and hepatocellular carcinoma. Current antiviral therapy does not effectively eradicate HBV and, thus, further investigation into the mechanisms employed by HBV to allow for invasion of host cells, is critical for the development of novel therapeutic agents. Sodium-taurocholate cotransporting polypeptide (NTCP) has been identified as a functional receptor for HBV. However, the specific mechanism by which HBV and NTCP interact remains unclear. Herein we show that the expression of E-cadherin was upregulated in cells expressing HBV, while knockdown of E-cadherin in HepG2-NTCP cells, HepaRG cells and primary human hepatocytes served to significantly inhibit infection by HBV and HBV pseudotyped particles. Alternatively, exogenous E-cadherin expression was found to significantly enhance HBV uptake by HepaRG cells. Further, mechanistic studies identified glycosylated NTCP localized to the cell membrane via E-cadherin binding, which subsequently allowed for more efficient binding between NTCP and the preS1 of the large HBV surface proteins. E-cadherin was also found to play a key role in establishing and maintaining hepatocyte polarity, which is essential for efficient HBV infection. These observations suggest that E-cadherin facilitates HBV entry through regulation of NTCP distribution and hepatocyte polarity.\n\nAuthor SummaryHepatitis B Virus (HBV) still seriously endangers public health. It is very important to understand the mechanism of HBV invading host cells for developing new therapy target. Sodium-taurocholate cotransporting polypeptide (NTCP) is the key receptor mediating HBV invasion, while other molecules also exhibit important roles in ensuring efficient and productive HBV infection. This study reports that E-cadherin facilitates HBV entry by directly interacting with glycosylated NTCP to mediate its distribution on the hepatocyte membrane and also affects the efficacy of HBV invasion by influncing hepatocyte polarity.

microbiology↗