The improvement of soybean seed carotenoid contents is indispensably important owing to its beneficial role to human health and nutrition.  However, the genetic architecture underlying soybean carotenoid biosynthesis remains largely unknown.  In the present study, we employed the next generation sequencing-based bulked-segregant analysis for identifying new genomic regions governing seed carotenoids in 1551 natural soybean accessions.  The genomic DNA samples of individual plants with extreme phenotype were pooled to form two bulks with high (50 accessions) and low (50 accessions) carotenoid contents for Illumina sequencing.  A total of 125.09 Gbp of clean bases and 89.82% of Q30 were obtained and the average alignment efficiency was 99.45% with average coverage depth of 62.20× and 99.75% genome coverage.  Based on the G' method analysis, a total of 16 candidate genomic loci with a total length 20.41 Mb were found to be related to the trait.  Of these loci, the most significant region displaying the highest elevated G'-value was found in chromosome 06 at a position of 18.53-22.67 Mb, and chromosome 19 at a genomic region intervals of 8.36-10.94, 12.06-13.79 and 18.45-20.26 Mbs, and were preferably taken to identify the key candidate genes.  In these regions, 250 predicted genes were found and analyzed to get 90 significantly enriched (P<0.05) gene ontology (GO)-terms.  Based on ANNOVAR analysis, 50 genes with non-synonymous and stopgained mutations were preferentially selected as potential candidate genes.  Of which, following their gene annotation function and high significant haplotype variation in various environments, five genes were identified as the most promising candidate genes regulating soybean seed carotenoid accumulation, and suggested for further functional validation studies.  Collectively, understanding the genetic bases of carotenoid pigments and identifying genes underpinning carotenoid accumulation via bulked-segregant analysis sequencing (BSA-seq) approach provide new insight for exploring future molecular breeding of high carotenoid content in soybean cultivars.

Pluripotent stem cells (PSCs) are useful for developmental and translational research because they have the potential to differentiate into all cell types of an adult individual. Pigs are one of the most important domestic ungulates, commonly used for food and as bioreactors. Generating stable pluripotent porcine PSC lines remains challenging. So far, the pluripotency gene network of porcine PSCs is poorly understood. Here we found that TBX3-derived induced pluripotent stem cells (iPSCs) closely resemble porcine 4-cell embryos with the capacity of totipotent-like stem cells (TLSCs). Interestingly, our data suggest that TBX3 facilitates the activation of H3K4me3 methyltransferase, specifically MLL1. Subsequent investigations revealed that the porcine 4-cell specific gene, MCL1, is a key downstream effector of the TBX3-MLL1 axis. Together, our study of the TBX3 regulatory network is helpful in the understanding of the totipotency characteristics of pigs.

Sulforaphane (SFN), a naturally occurring isothiocyanate found in cruciferous vegetables, is known for its anti-inflammatory and antioxidant effects in the body. However, whether its dietary addition impact porcine liver health, and if so, by which mechanims remains unclear. In this study, the diet of growing pigs was supplemented with 1 g kg^-1 SFN and was found to improve growth performance and hepatocellular proliferation. Further analyses revealed that SFN decreased hepatic and serum malondialdehyde levels, while increasing glutathione peroxidase (GSH-PX) activity in the liver. Transcriptomic and proteomic studies demonstrated that SFN down-regulated multiple pathways, including oxidative phosphorylation, inflammatory responses, IL-6-JAK-STAT3 signaling, and TNFα signaling via NFκB. Meanwhile, it upregulated NRF2/GPX4/HO-1 expression and reduced IL-6 and TNFα expression. Mechanistic studies identified potential NR1D1 and NRF2 binding elements in the promoters of the GPX4 and HO-1 genes in the liver. Furthermore, Metabolomic profiling revealed a decline in serum β-hydroxybutyrate levels after the administration of SFN, while further analysis confirmed that SFN enhanced a type of epigenetic modification in the liver, lysine β-hydroxybutyrylation (Kbhb).  These results highlight SFN protective roles against liver inflammation and oxidative damage and propose a novel mechanism involving NRF2 and NR1D1 synergy, with SFN’s promotion of hepatic Kbhb necessitating further exploration.