Feed cost accounts for approximately 65–75% of overall commercial pork production costs. Therefore, improving the feed efficiency of pig production is important. In this study, 12 individuals with either extremely high (HE) or low (LE) feed efficiency were selected from 225 Duroc × (Landrace × Yorkshire) (DLY) pigs. After the pigs were slaughtered, we collected small intestine mucosal tissue. Next, RNA sequencing (RNA-seq) analysis was used to reveal the presence and quantity of genes expressed between these extremely HE- and LE-groups. We found 433 significantly differentially expressed genes (DEGs) between the HE- and LE-groups. Of these, 389 and 44 DEGs were upregulated and downregulated in the HE-group, respectively. An enrichment analysis showed that the DEGs were mainly enriched in functions related to apical plasma membrane composition, transporter activity, transport process and hormone regulation of digestion and absorption. Protein network interaction and gene function analyses revealed that SLC2A2 was an important candidate gene for FE in pigs, which may give us a deeper understanding of the mechanism of feed efficiency. Furthermore, some significant DEGs identified in the current study could be incorporated into artificial selection programs for increased feeding efficiency in pigs.

Somatic cell nuclear transfer (SCNT) is the only method known to rapidly reprogram differentiated cells into totipotent embryos. Most cloned embryos become arrested before implantation and the details of the underlying molecular mechanism remain largely unknown. Dynamic regulation of the transcriptome is a key molecular mechanism driving early embryonic development. Here, we report comprehensive transcriptomic analysis of cloned embryos (from Laiwu and Duroc pigs) and in vivo fertilized embryos (from Duroc pigs) using RNA-sequencing. Comparisons between gene expression patterns were performed according to differentially expressed genes, specific-expressed genes, first-expressed genes, pluripotency genes and pathway enrichment analysis. In addition, we closely analyzed the improperly expressed histone lysine methyltransferases and histone lysine demethylases during cell reprogramming in cloned embryos. In summary, we identified altered gene expression profiles in porcine cloned pre-implantation embryos in comparison to normal in vivo embryos. Our findings provide a substantial framework for further discovery of the epigenetic reprogramming mechanisms in porcine SCNT embryos.

Feed efficiency is an economically important trait controlled by multiple genes in pigs. The small intestine is the main organ of digestion and nutrient absorption. To explore the biological processes by which small intestine proteomics affects feed efficiency (FE), we investigated the small intestinal tissue proteomes of high-FE and low-FE pigs by the isobaric tag for relative and absolute quantification (iTRAQ) method. In this study, a total of 225 Duroc × (Landrace × Yorkshire) (DLY) commercial pigs were ranked according to feed efficiency, which ranged from 30 kg to 100 kg, and six pigs with extreme phenotypes were selected, three in each of the high and low groups. A total of 1219 differentially expressed proteins (DEPs) were identified between the high-FE and low-FE groups (fold change ≥1.2 or ≤0.84; p ≤ 0.05), of which 785 were upregulated, and 484 were downregulated. Enrichment analysis indicated that the DEPs were mainly enriched in actin filament formation, microvilli formation, and small intestinal movement pathways. Protein functional analysis and protein interaction networks indicated that RHOA, HCLS1, EZR, CDC42, and RAC1 were important proteins that regulate FE in pigs. This study provided new insights into the important pathways and proteins involved in feed efficiency in pigs.

Purpose: Prenatal phenotypic manifestations of genetic disorders associated with NSD2 variants remain poorly characterized. This study presents our institutional experience with the prenatal diagnosis of NSD2 ‐associated genetic disorders, specifically Rauch–Steindl syndrome (RAUST), aiming to improve understanding of both the molecular and clinical features of RAUST. Methods: We performed a retrospective analysis of six fetuses and one adult diagnosed with RAUST at our institution and thoroughly reviewed the prenatal ultrasound reports of six fetuses. Prenatal and postnatal phenotypes of RAUST cases were summarized alongside findings from previously published literature. Correlations between NSD2 variant locations, variant types, and phenotypes were analyzed. Additionally, protein modeling was used to visualize structural changes in NSD2 protein before and after C‐terminal variants. We integrated single‐cell transcriptomic and gene expression data from multiple public databases to investigate spatiotemporal expression patterns of NSD2 during human fetal development. Results: Fetal growth restriction (FGR) was the most prevalent prenatal manifestation in RAUST fetuses, followed by microcephaly. Bilateral renal hypoplasia emerged as a novel prenatal ultrasonographic feature. Postnatally, speech and motor developmental delays were the most commonly reported phenotypes, followed by physical developmental delays and intellectual disability. Genotype‐phenotype correlation analysis revealed an association between N‐terminal truncating variants in NSD2 and impaired fetal growth parameters. Notably, C‐terminal truncating variants—predicted not to directly impact NSD2 functional domains—also exerted disease‐causing effects. Conclusion: This study provides a comprehensive analysis of prenatal phenotypes in RAUST cases, enriching the prenatal phenotypic spectrum of the disease and facilitating early diagnosis and clinical management of RAUST. Furthermore, our genotype‐phenotype correlation findings lay a foundational basis for future research into the complex molecular mechanisms underlying NSD2 ‐associated genetic disorders.