BackgroundUnderstanding the host impact on its symbiotic microbiota is important in redirecting the rumen microbiota and thus improving animal performance. The current study aimed to understand how rumen microbiota were altered and re-established after being emptied and receiving content from donor, thus to understand the impact of such process on rumen microbial fermentation and to explore the microbial phylotypes with higher manipulation potentials.ResultsIndividual animal had strong effect on the re-establishment of the bacterial community according to the observed profiles detected by both fingerprinting and pyrosequencing. Most of the bacterial profile recovery patterns and extents at genus level varied among steers; and each identified bacterial genus responded to transfaunation differently within each host. Coriobacteriaceae, Coprococcus, and Lactobacillus were found to be the most responsive and tunable genera by exchanging rumen content. Besides, the association of 18 bacterial phylotypes with host fermentation parameters suggest that these phylotypes should also be considered as the regulating targets in improving host feed efficiency. In addition, the archaeal community had different re-establishment patterns for each host as determined by fingerprint profiling: it was altered after receiving non-native microbiome in some animals, while it resumed its original status after the adaptation period in the other ones.ConclusionsThe highly individualized microbial re-establishment process suggested the importance of considering host genetics, microbial functional genomics, and host fermentation/performance assessment when developing effective and selective microbial manipulation methods for improving animal feed efficiency.Electronic supplementary materialThe online version of this article (10.1186/s40168-018-0447-y) contains supplementary material, which is available to authorized users.
The deposition of intramuscular (IM) and subcutaneous (SC) fat is an important trait influencing pork quality. Understanding the genetic differences between these two types of adipose tissues is consequently of great importance for pig breeding. Here, we established primary cultures of IM and SC adipocytes from Jiaxing black pigs. The microRNA (miRNA) expression profiles of the two types of adipocytes were obtained by RNA-seq. A total of 741 miRNAs were identified in IM and SC adipocytes, including 155 significant differentially expressed (SDE) miRNAs. According to gene ontology and Kyoto Encyclopedia of Genes analysis, the target genes of the SDE miRNAs were enriched in categories and pathways related to transcriptional regulation, fatty acid biosynthesis, as well as the MAPK and PI3K/Akt pathways. Notably, miR-206 expression was 36-fold higher in IM adipocytes than in SC adipocytes. The overexpression of miR-206 in IM and SC adipocytes decreased cell proliferation and triglyceride accumulation. Luciferase activity assays and quantitative polymerase chain reaction confirmed that miR-206 regulates adipocyte proliferation by targeting STARD7 and inhibits adipogenesis by repressing Krüppel-like factor 4 (KLF4) expression. Accordingly, the effect of miR-206 mimics was attenuated by the overexpression of KLF4 in adipocytes. Taken together, we identified the expression profiles of miRNAs in adipocytes, which revealed that miR-206 acts as a suppressor of adipogenesis.
Increasing intramuscular (IM) fat while concomitantly decreasing subcutaneous (SC) fat content is one major goal of pig breeding. Identifying genes involved in lipid metabolism is critical for this goal. Galectin-12 (LGALS12) has been proven to be an important regulator of fat deposition in mouse models; however, the effect and regulatory mechanisms of LGALS12 on porcine adipogenesis are still unknown. In this study, the effects of LGALS12 on fat deposition were explored with primary culture of porcine SC and IM adipocytes. Analysis of LGALS12 expression across different tissues revealed that LGALS12 was predominantly expressed in adipose tissue. The LGALS12 expression patterns across stages of adipocyte differentiation were also evaluated, with differences observed between SC and IM fat. Small interfering RNA (siRNA) of LGALS12 was designed and transfected into porcine adipocytes derived from SC and IM fat. After transfection, the expression level of LGALS12 was significantly reduced, and the number of lipid droplets was reduced in adipocytes from both SC and IM fat. Simultaneously, the levels of adipogenic markers, including PPARγ and aP2, were decreased, whereas hydrolysis markers, including adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), were increased. Furthermore, the activation of lipolysis signals, such as the phosphorylation of PKA and Erk1/2, were observed with LGALS12 knockdown in terminally differentiated adipocytes from both SC and IM sources. Taken together, these results suggest that LGALS12 knockdown can inhibit adipogenesis of porcine adipocytes by downregulating lipogenic genes and activating the PKA-Erk1/2 signaling pathway.
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