Bitter gourd (Momordica charantia) is a popular cultivated vegetable in Asian and African countries. To reveal the characteristics of the genomic structure, evolutionary trajectory, and genetic basis underlying the domestication of bitter gourd, we performed whole-genome sequencing of the cultivar Dali-11 and the wild small-fruited line TR and resequencing of 187 bitter gourd germplasms from 16 countries. The major gene clusters (Bi clusters) for the biosynthesis of cucurbitane triterpenoids, which confer a bitter taste, are highly conserved in cucumber, melon, and watermelon. Comparative analysis among cucurbit genomes revealed that the Bi cluster involved in cucurbitane triterpenoid biosynthesis is absent in bitter gourd. Phylogenetic analysis revealed that the TR group, including 21 bitter gourd germplasms, may belong to a new species or subspecies independent from M. charantia. Furthermore, we found that the remaining 166 M. charantia germplasms are geographically differentiated, and we identified 710, 412, and 290 candidate domestication genes in the South Asia, Southeast Asia, and China populations, respectively. This study provides new insights into bitter gourd genetic diversity and domestication and will facilitate the future genomics-enabled improvement of bitter gourd.

This experiment was conducted to evaluate the effects of bile acids (BAs) on the growth performance and lipid metabolism of broilers fed with different energy level diets. 480 one-day-old Arbor Acres broilers (45.01 ± 0.26 g) were allotted to a 2 × 2 factorial design with 2 levels of energy (basal or high-energy level) and 2 levels of BAs (with or without BAs supplementation), resulting in 4 groups of 8 replicates; the experiment lasted 42 d. High-energy diets decreased the feed/gain ratio (F/G) from 1 to 21 d (P < 0.05), and increased the liver index and abdominal fat percentage at 42 d (P < 0.05). The serum total triglyceride (TG) and high-density lipoprotein cholesterol at 42 d were increased by high-energy diets (P < 0.05), while the hepatic lipoprotein lipase (LPL) activity at 21 and 42 d was decreased (P < 0.05). BAs supplementation increased the body weight at 21 d and decreased the F/G during entire period (P < 0.05), as well as improved the carcass quality reflected by decreased abdominal fat percentage at 42 d and increased breast muscle percentage at 21 and 42 d (P < 0.05). The serum TG at 21 and 42 d were decreased by BAs (P < 0.05), and the hepatic LPL activity at 42 d was increased (P < 0.05). In addition, high-energy diets increased the expression of sterol regulatory element binding transcription factor 1, acetyl-CoA carboxylase, and fatty acid synthase (P < 0.05), while BAs diets decreased these genes expression (P < 0.05). Moreover, BAs supplementation also increased the expression of carnitine palmitoyltransferase 1 (P < 0.05), which was increased in high-energy groups (P < 0.05). In conclusion, BAs supplementation could increase growth performance, elevate carcass quality, and improve lipid metabolism in broilers.

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AKT/GSK-3β/β-catenin signaling pathway plays an important role in the progression of colorectal cancer (CRC). Toosendanin (TSN) is a triterpenoid extracted from the bark or fruits of Melia toosendan Sieb et Zucc and possesses antitumour effects on various human cancer cells. However, its effect on CRC remains poorly understood. The present study investigated the effect of TSN on CRC SW480 cells and the AKT/GSK-3β/β-catenin signaling. Proliferation assay, flow cytometry and Hoechst 33342 nuclear staining demonstrated TSN dose-dependently inhibited cell viability and induced cell apoptosis as well as cell cycle arrest in S phase. Confocal laser scanning microscope showed β-catenin transferred to the outside of the nucleus in TSN-treated cells. Quantitative real-time PCR and western blot analysis found that TSN effectively modulated molecules related to apoptosis and AKT/GSK-3β/β-catenin signaling. Moreover, TSN administration significantly inhibited CRC growth in a mouse tumor xenograft model. In conclusion, our findings indicate that TSN inhibits growth and induces apoptosis in CRC cells through suppression of AKT/GSK-3β/β-catenin pathway, suggesting that TSN may have potential for use in CRC treatment.