Quinoa (Chenopodium quinoa Willd.) was known as the “golden grain” by the native Andean people in South America, and has been a source of valuable food over thousands of years. It can produce a variety of secondary metabolites with broad spectra of bioactivities. At least 193 secondary metabolites from quinoa have been identified in the past 40 years. They mainly include phenolic acids, flavonoids, terpenoids, steroids, and nitrogen-containing compounds. These metabolites exhibit many physiological functions, such as insecticidal, molluscicidal and antimicrobial activities, as well as various kinds of biological activities such as antioxidant, cytotoxic, anti-diabetic and anti-inflammatory properties. This review focuses on our knowledge of the structures, biological activities and functions of quinoa secondary metabolites. Biosynthesis, development and utilization of the secondary metabolites especially from quinoa bran were prospected.

Cyclic peptides are cyclic compounds formed mainly by the amide bonds between either proteinogenic or non-proteinogenic amino acids. This review highlights the occurrence, structures and biological activities of fungal cyclic peptides (excluding cyclodipeptides, and peptides containing ester bonds in the core ring) reported until August 2017. About 293 cyclic peptides belonging to the groups of cyclic tri-, tetra-, penta-, hexa-, hepta-, octa-, nona-, deca-, undeca-, dodeca-, tetradeca-, and octadecapeptides as well as cyclic peptides containing ether bonds in the core ring have been isolated from fungi. They were mainly isolated from the genera Aspergillus, Penicillium, Fusarium, Acremonium and Amanita. Some of them were screened to have antimicrobial, antiviral, cytotoxic, phytotoxic, insecticidal, nematicidal, immunosuppressive and enzyme-inhibitory activities to show their potential applications. Some fungal cyclic peptides such as the echinocandins, pneumocandins and cyclosporin A have been developed as pharmaceuticals.

A study was conducted to evaluate the main effects of dietary nitrate adaptation by cattle and alfalfa cell wall to starch ratio in in vitro substrates on nitrate disappearance and nitrite and volatile fatty acid (VFA) concentrations, as well as hydrogen (H 2 ) and methane (CH 4 ) accumulations. Rumen fluid from steers fed diets containing urea or nitrate was added into in vitro incubations containing sodium nitrate as the sole nitrogen source and 20 cell wall : 80 starch or 80 cell wall : 20 starch as the carbohydrate source. The results showed that during 24 h incubation, rumen fluid inoculums from steers adapted to dietary nitrate resulted in more rapid nitrate disappearance by 6 h of incubation (P , 0.01), no significant effect on nitrite concentration and diminished CH 4 accumulation (P , 0.05). Cell wall to starch ratio did not affect nitrate disappearance, CH 4 accumulation and total VFA concentration. The higher cell wall ratio had the lower total gas production and H 2 concentration (P , 0.05). Ammonia-N (NH 3 -N) concentration increased because of adaptation of donors to nitrate feeding (P , 0.05). Nitrate adaptation did not alter total VFA concentration, but increased acetate, and decreased propionate and butyrate molar proportions (P , 0.01).

Acidovorax citrulli causes seedling blight and bacterial fruit blotch (BFB) of cucurbits, a serious disease threat to cucurbit seed and fruit production worldwide. Despite its economic importance, current knowledge on the biology and pathology of A. citrulli is limited. This work studies a mini-Tn5 mutant, MJ22-3, that showed reduced virulence on melon seedlings. The gene disrupted by Tn5 was identified as leuB, which encodes a putative 3-isopropylmalate dehydrogenase, an enzyme that appears to be essential for leucine biosynthesis. The leuB gene in-frame deletion mutant MDleuB, as well as the Tn5-inserted mutant MJ22-3, failed to grow in minimal medium without leucine and exhibited reduced swimming motility; however, the mutations had no effect on biofilm formation or induction of the hypersensitive response on tobacco (Nicotiana tabacum). When inoculated at a low cell density (10 4 CFU mL À1), the leuB gene mutants showed a significantly slower growth rate and attenuated virulence on melon cotyledons compared to the wildtype MH21. However, inoculations with the mutants at high concentration (10 8 CFU mL À1 ), or low concentration (10 4 CFU mL À1 ) inoculations supplemented with 0Á01% leucine resulted in growth rates and disease severities similar to that of the wildtype MH21. The results suggest that leucine biosynthesis is essential for both in vivo growth and full virulence of A. citrulli MH21 on melon seedlings.

Xanthomonas campestris pv. campestris (Xcc) can cause black rot in cruciferous plants worldwide. Two‐component systems (TCSs) are key for bacterial adaptation to various environments, including hosts. VemR is a TCS response regulator and crucial for Xcc motility and virulence. Here, we report that RavA is the cognate histidine kinase (HK) of VemR and elucidate the signalling pathway by which VemR regulates Xcc motility and virulence. Genetic analysis showed that VemR is epistatic to RavA. Using bacterial two‐hybrid experiments and pull‐down and phosphorylation assays, we found that RavA can interact with and phosphorylate VemR, suggesting that RavA is the cognate HK of VemR. In addition, we found that RpoN2 and FleQ are epistatic to VemR in regulating bacterial motility and virulence. In vivo and in vitro experiments demonstrated that VemR interacts with FleQ but not with RpoN2. RavA/VemR regulates the expression of the flagellin‐encoding gene fliC by activating the transcription of the rpoN2‐vemR‐fleQ and flhF‐fleN‐fliA operons. In summary, our data show that the RavA/VemR TCS regulates FleQ activity and thus influences the expression of motility‐related genes, thereby affecting Xcc motility and virulence. The identification of this novel signalling pathway will deepen our understanding of Xcc–plant interactions.