Transcriptome analysis of Rhizopus oryzae seed pellet formation using triethanolamine

Rhizopus oryzae (R. oryzae) can effectively produce organic acids, and its pellet formation in seed cultures has been shown to significantly enhance subsequent fermentation processes. Despite advances in strain development, simple and effective methods for inducing pellet morphology and a basic understanding of the mechanisms controlling this process could facilitate substantial increases in efficiency and product output. Here, we report that 1.5% triethanolamine (TEOA) in seed culture medium can activate the growth of R. oryzae spores in compact and uniform pellets which is optimal for fermentation conditions. Analysis of fermentation kinetics showed that the production of fumaric and L-malic acid increases 293% and 177%, respectively. Transcriptomic analysis revealed that exposure of R. oryzae to 1.5% TEOA during the seed culture activated the phosphatidylinositol and mitogen-activated protein kinase signaling pathways. Theses pathways subsequently stimulated the downstream carbohydrate-active synthases and hydrolases that required for cell wall component synthesis and reconstruction. Our results thus provide insight into the regulatory pathways controlling pellet morphology germane to the viability of seed cultures, and provide valuable reference data for subsequent optimization of organic acid fermentation by R. oryzae.

Integrated de novo Analysis of Transcriptional and Metabolic Variations in Salt-Treated Solenostemma argel Desert Plants

Solenostemma argel (Delile) Hayne is a desert plant that survives harsh environmental conditions with several vital medicinal properties. Salt stress is a major constraint limiting agricultural production around the globe. However, response mechanisms behind the adaptation of S. argel plants to salt stress are still poorly understood. In the current study, we applied an omics approach to explore how this plant adapts to salt stress by integrating transcriptomic and metabolomic changes in the roots and leaves of S. argel plants under salt stress. De novo assembly of transcriptome produced 57,796 unigenes represented by 165,147 transcripts/isoforms. A total of 730 differentially expressed genes (DEGs) were identified in the roots (396 and 334 were up- and down-regulated, respectively). In the leaves, 927 DEGs were identified (601 and 326 were up- and down-regulated, respectively). Gene ontology and Kyoto Encyclopedia of Genes And Genomes pathway enrichment analyses revealed that several defense-related biological processes, such as response to osmotic and oxidative stress, hormonal signal transduction, mitogen-activated protein kinase signaling, and phenylpropanoid biosynthesis pathways are the potential mechanisms involved in the tolerance of S. argel plants to salt stress. Furthermore, liquid chromatography-tandem mass spectrometry was used to detect the metabolic variations of the leaves and roots of S. argel under control and salt stress. 45 and 56 critical metabolites showed changes in their levels in the stressed roots and leaves, respectively; there were 20 metabolites in common between the roots and leaves. Differentially accumulated metabolites included amino acids, polyamines, hydroxycinnamic acids, monolignols, flavonoids, and saccharides that improve antioxidant ability and osmotic adjustment of S. argel plants under salt stress. The results present insights into potential salt response mechanisms in S. argel desert plants and increase the knowledge in order to generate more tolerant crops to salt stress.

Selenoproteins Protect Against Avian Liver Necrosis by Metabolizing Peroxides and Regulating Receptor Interacting Serine Threonine Kinase 1/Receptor Interacting Serine Threonine Kinase 3/Mixed Lineage Kinase Domain-Like and Mitogen-Activated Protein Kinase Signaling

Liver necroptosis of chicks is induced by selenium (Se)/vitamin E (VE) deficiencies and may be associated with oxidative cell damage. To reveal the underlying mechanisms of liver necrosis, a pool of the corn–soy basal diet (10 μg Se/kg; no VE added), a basal diet plus all-rac-α-tocopheryl acetate (50 mg/kg), Se (sodium selenite at 0.3 mg/kg), or both of these nutrients were provided to day-old broiler chicks (n = 40/group) for 6 weeks. High incidences of liver necrosis (30%) of chicks were induced by –SE–VE, starting at day 16. The Se concentration in liver and glutathione peroxidase (GPX) activity were decreased (P < 0.05) by dietary Se deficiency. Meanwhile, Se deficiency elevated malondialdehyde content and decreased superoxide dismutase (SOD) activity in the liver at weeks 2 and 4. Chicks fed with the two Se-deficient diets showed lower (P < 0.05) hepatic mRNA expression of Gpx1, Gpx3, Gpx4, Selenof, Selenoh, Selenok, Selenom, Selenon, Selenoo, Selenop, Selenot, Selenou, Selenow, and Dio1 than those fed with the two Se-supplemented diets. Dietary Se deficiency had elevated (P < 0.05) the expression of SELENOP, but decreased the downregulation (P < 0.05) of GPX1, GPX4, SELENON, and SELENOW in the liver of chicks at two time points. Meanwhile, dietary Se deficiency upregulated (P < 0.05) the abundance of hepatic proteins of p38 mitogen-activated protein kinase, phospho-p38 mitogen-activated protein kinase, c-Jun N-terminal kinase, phospho-c-Jun N-terminal kinase, extracellular signal-regulated kinase, phospho-mitogen-activated protein kinase, receptor-interacting serine-threonine kinase 1 (RIPK1), receptor-interacting serine-threonine kinase 3 (RIPK3), and mixed lineage kinase domain-like (MLKL) at two time points. In conclusion, our data confirmed the differential regulation of dietary Se deficiency on several key selenoproteins, the RIPK1/RIPK3/MLKL, and mitogen-activated protein kinase signaling pathway in chicks and identified new molecular clues for understanding the etiology of nutritional liver necrosis.