De-domestication is a unique evolutionary process by which domesticated crops are converted into ‘wild predecessor like' forms. Weedy rice (Oryza sativa f. spontanea) is an excellent model to dissect the molecular processes underlying de-domestication. Here, we analyse the genomes of 155 weedy and 76 locally cultivated rice accessions from four representative regions in China that were sequenced to an average 18.2 × coverage. Phylogenetic and demographic analyses indicate that Chinese weedy rice was de-domesticated independently from cultivated rice and experienced a strong genetic bottleneck. Although evolving from multiple origins, critical genes underlying convergent evolution of different weedy types can be found. Allele frequency analyses suggest that standing variations and new mutations contribute differently to japonica and indica weedy rice. We identify a Mb-scale genomic region present in weedy rice but not cultivated rice genomes that shows evidence of balancing selection, thereby suggesting that there might be more complexity inherent to the process of de-domestication.

Taraxasterol, a pentacyclic-triterpene compound, is one of the main active components isolated from the traditional Chinese medicinal herb Taraxacum. The objective of this study is to evaluate the protective effects of taraxasterol and its possible underlying mechanisms against ethanol-induced liver injury in mice. ICR mice were fed with Lieber-DeCarli diet containing 5% ethanol for 10 d and then challenged with a single dose of 20% ethanol (5 g/kg BW) by intragastric administration. The mice were intragastrically treated daily with taraxasterol (2.5, 5, and 10 mg/kg). Tiopronin was used as a positive control. The liver index was calculated, and the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), triglyceride (TG), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) in sera were detected. The contents of reactive oxygen species (ROS), malondialdehyde (MDA), and glutathione (GSH) and the activity of superoxide dismutase (SOD) in the livers were measured. The histopathological changes of liver tissues were observed by hematoxylin and eosin (H&E) staining. The protein expression levels of hepatic cytochrome P450 2E1 (CYP2E1), nuclear factor erythroid 2-related factor 2 (Nrf2), antioxidant protein heme oxygenase-1 (HO-1), and nuclear factor-kappa B (NF-κB) signaling pathway in liver tissues were detected by immunohistochemistry and Western blot methods. Taraxasterol significantly reduced the ethanol-induced increases of liver index, ALT, AST, and TG levels in sera and TG and MDA contents in the livers and hepatic ROS production and suppressed the ethanol-induced decreases of hepatic GSH level and SOD activity. Taraxasterol also significantly inhibited the secretion of proinflammatory cytokines TNF-α and IL-6 induced by ethanol. In addition, taraxasterol improved the liver histopathological changes in mice with ethanol-induced liver injury. Further studies revealed that taraxasterol significantly inhibited the ethanol-induced upregulation of CYP2E1, increased the ethanol-induced downregulation of Nrf2 and HO-1, and inhibited the degradation of inhibitory kappa Bα (IκBα) and the expression level of NF-κB p65 in liver tissues of ethanol-induced mice. These findings suggest that taraxasterol possesses the potential protective effects against ethanol-induced liver injury in mice by exerting antioxidative stress and anti-inflammatory response via CYP2E1/Nrf2/HO-1 and NF-κB signaling pathways.

The fall armyworm (Spodoptera frugiperda) is a lepidopteran insect pest that causes huge economic losses. This notorious insect pest has rapidly spread over the world in the past few years. However, the mechanisms of rapid dispersal are not well understood. Here, we report a chromosome-level assembled genome of the fall armyworm, named the ZJ-version, using PacBio and Hi-C technology. The sequenced individual was a female collected from the Zhejiang province of China and had high heterozygosity. The assembled genome size of ZJ-version was 486 Mb, containing 361 contigs with an N50 of 1.13 Mb. Hi-C scaffolding further assembled the genome into 31 chromosomes and a portion of W chromosome, representing 97.4% of all contigs and resulted in a chromosome-level genome with scaffold N50 of 16.3 Mb. The sex chromosomes were identified by genome resequencing of a single male pupa and a single female pupa. About 28% of the genome was annotated as repeat sequences, and 22,623 protein-coding genes were identified. Comparative genomics revealed the expansion of the detoxification-associated gene families, chemoreception-associated gene families, nutrition metabolism and transport system gene families in the fall armyworm. Transcriptomic and phylogenetic analyses focused on these gene families revealed the potential roles of the genes in polyphagia and invasion of fall armyworm. The high-quality of the fall armyworm genome provides an important genomic resource for further explorations of the mechanisms of polyphagia and insecticide resistance, as well as for pest management of fall armyworm. K E Y W O R D S chromosome-level genome, comparative genomics, fall armyworm, insecticide resistance, polyphagia | 1051 XIAO et Al.

Gut microbiota play an important role in maintaining intestinal health and are involved in the metabolism of carbohydrates, lipids, and amino acids. Recent studies have shown that the central nervous system (CNS) and enteric nervous system (ENS) can interact with gut microbiota to regulate nutrient metabolism. The vagal nerve system communicates between the CNS and ENS to control gastrointestinal tract functions and feeding behavior. Vagal afferent neurons also express receptors for gut peptides that are secreted from enteroendocrine cells (EECs), such as cholecystokinin (CCK), ghrelin, leptin, peptide tyrosine tyrosine (PYY), glucagon-like peptide-1 (GLP-1), and 5-hydroxytryptamine (5-HT; serotonin). Gut microbiota can regulate levels of these gut peptides to influence the vagal afferent pathway and thus regulate intestinal metabolism via the microbiota-gut-brain axis. In addition, bile acids, short-chain fatty acids (SCFAs), trimethylamine-N-oxide (TMAO), and Immunoglobulin A (IgA) can also exert metabolic control through the microbiota-gut-liver axis. This review is mainly focused on the role of gut microbiota in neuroendocrine regulation of nutrient metabolism via the microbiota-gut-brain-liver axis.2 of 21 formate, acetate, propionate, and butyrate, which are related to maintaining intestinal epithelium and permeability [11]. Further, SCFAs regulate glucose and lipid metabolism as well as immune and inflammatory responses [12,13]. Hence, gut microbiota also plays an important role in immune systems, inflammation, and cancer prevention of the host [14,15]. The enteric nervous system (ENS) is reported to be involved in intestinal metabolic regulation, and enteric neurons and intestinal neurotransmitters play an important role in ENS regulation [16][17][18]. The gut contains full ENS reflex circuits, such as motor neurons, interneurons, and sensory neurons, and these neurons transfer information between the ENS and central nervous system (CNS). The vagal nerve pathway communicates between the CNS and ENS, which has remarkable impact on regulating gastrointestinal tract functions and feeding behavior [19,20]. Thus, the vagal nerve system is also involved in intestinal metabolic regulation through the gut-brain axis. Vagal afferent neurons express receptors for gut peptides, such as cholecystokinin (CCK), ghrelin, leptin, peptide tyrosine tyrosine (PYY), glucagon-like peptide-1 (GLP-1), 5-hydroxytryptamine (5-HT) and so on, which are secreted from enteroendocrine cells (EECs) [20][21][22]. When vagal afferent neurons sense these types of gut peptides, the corresponding gut information will transfer to the CNS and exert various reactions. At the same time, gut microbiota can regulate these gut peptides, such as CCK, ghrelin, leptin, PYY, GLP-1, 5-HT levels to influence vagal afferent pathway, and then regulated intestinal metabolic metabolism via the microbiota-gut-brain axis [23][24][25].The importance of the gut-brain axis in human health and disease has been known for a long period. However, it has only been re...