Considerable difference in artemisinin and its direct precursors, artemisinic acid and dihydroartemisinic acid, was detected between two chemotypes within the species Artemisia annua (A. annua). These two chemotypes showed differential metabolic response to methyl jasmonate (MeJA) elicitation. Exogenous application of MeJA resulted in an accumulation of dihydroartemisinic acid and artemisinin in Type I plants. In Type II plants, however, artemisinic acid and artemisinin level decreased dramatically under MeJA elicitation. Squalene and other sesquiterpenes, (e.g., caryophyllene, germacrene D), were stimulated by MeJA in both chemotypes. The effect of MeJA elicitation was also studied at the transcription level. Real time RT-PCR analysis showed a coordinated activation of most artemisinin pathway genes by MeJA in Type I plants. The lack of change in cytochrome P450 reductase (CPR) transcript in Type I plants indicates that the rate-limiting enzymes in artemisinin biosynthesis have yet to be identified. Other chemotype-specific electron donor proteins likely exist in A. annua to meet the demand for P450-mediated reactions in MeJA-mediated cellular processes. In Type II plants, mRNA expression patterns of most pathway genes were consistent with the reduced artemisinin level. Intriguingly, the mRNA transcript of aldehyde dehydrogenase1 (ADHL1), an enzyme which catalyzes the oxidation of artemisinic and dihydroartemisinic aldehydes, was upregulated by MeJA. The differential metabolic response to MeJA suggests a chemotype-dependent metabolic flux control towards artemisinin and sterol production in the species A. annua.

Previous studies have shown that folate levels were decreased in patients with type 2 diabetes (T2D) and further lowered in T2D patients with cognitive impairment. However, whether folate deficiency could cause T2D and subsequent cognitive dysfunction is still unknown. The present study aimed to explore the effects of chronic folate deficiency (CFD) on glucose and lipid metabolism and cognitive function in mice. Seven-week-old mice were fed with either a CFD or control diet for 25 weeks. Serum folate was significantly reduced, whereas serum total homocysteine was significantly increased in the CFD group. Moreover, CFD induced obesity after a 6-week diet treatment, glucose intolerance and insulin resistance after a 16-week-diet treatment. In addition, CFD reduced the hepatic p-Akt/Akt ratio in response to acute insulin administration. Moreover, CFD increased serum triglyceride levels, upregulated hepatic Acc1 and Fasn mRNA expression, and downregulated hepatic Cd36 and ApoB mRNA expression. After a 24-week diet treatment, CFD induced anxiety-related activities and impairment of spatial learning and memory performance. This study demonstrates that folate deficiency could induce obesity, glucose and lipid metabolism disorders and subsequent cognitive dysfunction.

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Sacred lotus (Nelumbo nucifera) is an important aquatic ornamental plant which contains several diverse flower colors, but the underlying mechanisms of its flower coloration remain unclear. In this study, seven complementary DNA (cDNA) clones of genes involved in flavonoid biosynthesis, including chalcone synthase (CHS), chalcone isomerase (CHI), flavanone 3-hydroxylase (F3H), flavonoid 3′-hydroxylase (F3′H), flavonoid 3′,5′-hydroxylase (F3′5′H), dihydroflavonol 4-reductase (DFR), and anthocyanidin synthase (ANS), were isolated and characterized. Moreover, expression patterns of these seven genes and pigment profiles were investigated across four N. nucifera cultivars with different flower colors: Zhongguohongbeijing [ZGH (red)], Xinghuafen [XHF (pink)], Molingqiuse [MLQS (yellow)], and Zhufengcuiying [ZFCY (white)]. Real-time quantitative polymerase chain reaction (qRT-PCR) analysis showed that during flower development, transcripts of early biosynthetic genes (NnCHS, NnCHI, and NnF3H) were abundant at the early stage; noticeably, highest expression of NnCHI in MLQS probably induced abundant anthoxanthin synthesis and displayed yellow. Expression of late biosynthetic genes, especially NnDFR and NnANS, was generally consistent with change patterns of anthocyanins in ZGH and XHF, but NnF3′H was barely detectable in the pink cultivars. Meanwhile, negligible expression of NnDFR and NnANS was detected in MLQS and ZFCY, respectively, which blocked their colored anthocyanin biosynthesis. Spatial expression analysis revealed that most flavonoid biosynthetic genes were highly expressed in floral tissues, rather than leaves. These results suggest that in N. nucifera cultivars with different flower colors, flavonoid biosynthesis is differentially regulated by the expression of these flavonoid biosynthetic genes, among which, NnCHI, NnF3′H, NnDFR, and NnANS are supposed to be critical for pigment accumulation, and therefore, affect different flower coloration.

Background:Congenital myasthenic syndromes are a group of rare disorders that are clinically and genetically heterogeneous and caused by mutations in the genes encoding proteins of the neuromuscular junction. Here, we described a Chinese family that presented with phenotypes of classic slow-channel congenital myasthenic syndrome (SCCMS).Methods:Clinical characteristics and electrophysiological features of three patients from a Chinese family were examined, and next-generation sequencing followed by direct sequencing was carried out.Results:The patients revealed variability in clinical and electrophysiological features. However, weakness, scoliosis, and repetitive-compound muscle action potential were found in all affected members in the family. A heterozygous C>T missense mutation at nucleotide 865 in acetylcholine receptor epsilon-subunit (CHRNE) gene that causes a leucine-to-phenylalanine substitution at position 289 (L289F) was found.Conclusions:We reported a SCCMS family of Chinese origin. In the family, classical clinical phenotype with phenotypic variability among different members was found. Genetic testing could help diagnose this rare disease.