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Inflammatory Bowel Disease (IBD) is characterized by chronic inflammation of the gastrointestinal tract that associates with, among others, increased risk of colorectal cancer. There is a growing evidence that miRNAs have important roles in pathological processes, such as inflammation or carcinogenesis. Understanding the molecular mechanisms such as alterations in microRNAome upon chronic intestinal inflammation is critical for understanding the exact pathomechanism of IBD. Hence, we conducted a genome wide microRNAome analysis by applying miRNA-Seq in a rat model of experimental colitis, validated the data by QPCR, examined the expression of a selection of precursor and mature miRNAs, performed in depth biological interpretation using Ingenuity Pathway Analysis and tested the obtained results on samples derived from human patients. We identified specific, interdependent expression pattern of activator/repressor transcription factors, miRNAs and their direct targets in the inflamed colon samples. Particularly, decreased expression of the miR-200 family members (miR-200a/b/c,-141, and -429) and miR-27b correlates with the reduced level of their enhancers (HNF1B, E2F1), elevated expression of their repressors (ZEB2, NFKB1) and increased expression of their target genes (ZEB2, RUNX1). Moreover, the marked upregulation of six miR-27b target genes (IFI16, GCA, CYP1B1, RUNX1, MEF2C and MMP13) in the inflamed colon tissues is a possible direct consequence of the lack of repression due to the downregulated miRNA-27b expression. Our data indicate that changes in microRNAome are associated with the pathophysiology of IBD, consequently, microRNAs offer potential targets for the diagnosis, prognosis and treatment of IBD. [ABSTRACT FROM AUTHOR]

Inflammatory Bowel Disease (IBD) is characterized by chronic inflammation of the gastrointestinal tract that associates with, among others, increased risk of colorectal cancer. There is a growing evidence that miRNAs have important roles in pathological processes, such as inflammation or carcinogenesis. Understanding the molecular mechanisms such as alterations in microRNAome upon chronic intestinal inflammation is critical for understanding the exact pathomechanism of IBD. Hence, we conducted a genome wide microRNAome analysis by applying miRNA-Seq in a rat model of experimental colitis, validated the data by QPCR, examined the expression of a selection of precursor and mature miRNAs, performed in depth biological interpretation using Ingenuity Pathway Analysis and tested the obtained results on samples derived from human patients. We identified specific, interdependent expression pattern of activator/repressor transcription factors, miRNAs and their direct targets in the inflamed colon samples. Particularly, decreased expression of the miR-200 family members (miR-200a/b/c,-141, and -429) and miR-27b correlates with the reduced level of their enhancers (HNF1B, E2F1), elevated expression of their repressors (ZEB2, NFKB1) and increased expression of their target genes (ZEB2, RUNX1). Moreover, the marked upregulation of six miR-27b target genes (IFI16, GCA, CYP1B1, RUNX1, MEF2C and MMP13) in the inflamed colon tissues is a possible direct consequence of the lack of repression due to the downregulated miRNA-27b expression. Our data indicate that changes in microRNAome are associated with the pathophysiology of IBD, consequently, microRNAs offer potential targets for the diagnosis, prognosis and treatment of IBD.

Summary: Fat deposition is an important economic trait in farm animals. However, it is difficult to genetically improve intramuscular fat deposition via trait‐based cattle breeding. The main objectives of this study were to analyze the factors about beef flavor, and to detect functional microRNA (miRNA, miR) associated with intramuscular fat deposition in Yanbian cattle. Longissimus dorsi samples from six steers were separated into high‐ and low‐fat groups (n = 3 each) based on the marbling score, and transcriptomic analysis was performed using miRNA sequencing. A total of 33 miRNAs and 38 genes were found to be differentially expressed in the high‐ and low‐fat groups. Quantitative real‐time polymerase chain reaction was performed to validate the sequencing results. Integrated miRNA–mRNA analysis revealed that miRNA‐associated target genes were primarily associated with skeletal muscle development. However, some of the miRNAs (miR‐424 etc.) and genes (ATF3 etc.) were also associated with fat metabolism. A targeted relationship between miR‐22‐3p and the WFIKKN2 gene and its involvement in adipocyte differentiation were confirmed experimentally. The study findings may provide potential candidate molecular targets for the selection of cattle with improved meat quality. [ABSTRACT FROM AUTHOR]

Bovine tuberculosis is caused by infection with Mycobacterium bovis, which can also cause disease in a range of other mammals, including humans. Alveolar macrophages are the key immune effector cells that first encounter M. bovis and how the macrophage epigenome responds to mycobacterial pathogens is currently not well understood. Here, we have used chromatin immunoprecipitation sequencing (ChIP-seq), RNA-seq and miRNA-seq to examine the effect of M. bovis infection on the bovine alveolar macrophage (bAM) epigenome. We show that H3K4me3 is more prevalent, at a genome-wide level, in chromatin from M. bovis-infected bAM compared to control non-infected bAM; this was particularly evident at the transcriptional start sites of genes that determine programmed macrophage responses to mycobacterial infection (e.g. M1/M2 macrophage polarisation). This pattern was also supported by the distribution of RNA Polymerase II (Pol II) ChIP-seq results, which highlighted significantly increased transcriptional activity at genes demarcated by permissive chromatin. Identification of these genes enabled integration of high-density genome-wide association study (GWAS) data, which revealed genomic regions associated with resilience to infection with M. bovis in cattle. Through integration of these data, we show that bAM transcriptional reprogramming occurs through differential distribution of H3K4me3 and Pol II at key immune genes. Furthermore, this subset of genes can be used to prioritise genomic variants from a relevant GWAS data set.

For tree crops, shortening the juvenile phase is a vital strategy to advance fruit bearing and enhance the breeding efficiency. Walnut (Juglans regia L.) seedlings usually take at least eight to 10 years to flower, but early-flowering (EF) types can flower one or two years after planting. In this study, RNA sequencing (RNA-Seq) and microRNA sequencing (miRNA-Seq) were used for a transcriptome-wide analysis of gene and miRNA expression in hybrids of the Xinjiang EF walnut variety ‘Xinwen 81’ and later-flowering (LF) walnut. Based on a high-quality chromosome-scale reference genome, a total of 3009 differentially expressed genes (DEGs) were identified, of which 933 were upregulated (accounting for 31%) and 2076 were downregulated (accounting for 69%). DEGs were functionally annotated, and the flowering-related genes FLOWERING LOCUS T (FT), SUPPRESSOR OF OVEREXPRESSION OF CO 1 (SOC1), and LEAFY (LFY) showed remarkable upregulation in EF compared with in the LF walnut. In addition, miRNAs associated with floral transition were screened as candidates for flowering time regulation in the walnut. This work provides new insights into walnut floral transition, which may ultimately contribute to genetic improvement of the walnut.

Xenopus laevis survive severe dehydration during the summer months in their natural range. MicroRNA regulate translation of target mRNAs and have shown to be differentially expressed in response to dehydration in X. laevis. During dehydration, heart rate is elevated which appears to compensate for the reduced oxygen delivery capability due to increased hematocrit. We hypothesized that microRNAs would be differentially expressed in the heart to modulate gene expression levels in response to dehydration. The present study assessed changes in the microRNAome of X. laevis heart in response to severe dehydration (30% loss of body water) using microRNA-seq. We show that target genes are enriched for RNA, DNA, and transcription factor binding activities, cardiac muscle contraction, and glycolysis/gluconeogenesis. These results suggest that microRNAs contribute to gene expression reorganization in the heart in response to dehydration, putatively supporting the increased physiological demands and ATP production needs by the heart under these conditions. • Most differentially expressed microRNA are downregulated during dehydration. • Target genes are enriched for RNA, DNA, and transcription factor binding activities. • Nearly all glycolytic genes predicted to be less regulated by microRNA. [ABSTRACT FROM AUTHOR]

Marek's disease (MD) is a lymphoproliferative disease of domestic chickens caused by a cell-associated oncogenic alpha-herpesvirus, Marek's disease virus (MDV). Clinical signs of MD include bursal/thymic atrophy, neurologic disorders, and T cell lymphomas. MiRNAs play key roles in regulation of gene expression by targeting translational suppression or mRNA degradation. MDV encodes miRNAs that are associated with viral pathogenicity and oncogenesis. In this study, we performed miRNA sequencing in the bursal tissues, non-tumorous but viral-induced atrophied lymphoid organ, from control and infected MD-resistant and susceptible chickens at 21 days post infection. In addition to some known miRNAs, a minimum of 300 novel miRNAs were identified in each group that mapped to the chicken genome with no sequence homology to existing miRNAs in chicken miRbase. Comparative analysis identified 54 deferentially expressed miRNAs between the chicken lines that might shed light on underlying mechanism of bursal atrophy and resistance or susceptibility to MD. • MDV induces bursal atrophy and visceral tumors. • Comparative analysis of small RNA gene expression profiling identified more than 300 novel chicken miRNAs. • 54 differentially expressed known and novel miRNAs were identified between the control and infected chicken lines. • First report of its kind on miRNA profiling in a non-tumorous lymphoid organ that undergoes severe atrophy in MDV-infected chickens. • Complementary miRNA profiling in thymus might shed light on the role of miRNA in tumor development and lymphoid atrophy. [ABSTRACT FROM AUTHOR]

Bovine tuberculosis is caused by infection with Mycobacterium bovis , which can also cause disease in a range of other mammals, including humans. Alveolar macrophages are the key immune effector cells that first encounter M. bovis and how the macrophage epigenome responds to mycobacterial pathogens is currently not well understood. Here, we have used chromatin immunoprecipitation sequencing (ChIP-seq), RNA-seq and miRNA-seq to examine the effect of M. bovis infection on the bovine alveolar macrophage (bAM) epigenome. We show that H3K4me3 is more prevalent, at a genome-wide level, in chromatin from M. bovis -infected bAM compared to control non-infected bAM; this was particularly evident at the transcriptional start sites of genes that determine programmed macrophage responses to mycobacterial infection (e.g. M1/M2 macrophage polarisation). This pattern was also supported by the distribution of RNA Polymerase II (Pol II) ChIP-seq results, which highlighted significantly increased transcriptional activity at genes demarcated by permissive chromatin. Identification of these genes enabled integration of high-density genome-wide association study (GWAS) data, which revealed genomic regions associated with resilience to infection with M. bovis in cattle. Through integration of these data, we show that bAM transcriptional reprogramming occurs through differential distribution of H3K4me3 and Pol II at key immune genes. Furthermore, this subset of genes can be used to prioritise genomic variants from a relevant GWAS data set. [ABSTRACT FROM AUTHOR]

The article discusses a monolayer of endothelial cells line brain capillaries known as Blood-brain barrier (BBB). Particular focus is given to the functions of BBB and its role in the pathophysiological consequences in the brain. Also discussed are the microRNA analysis, BBB transcriptomics data and pathways that regulate BBB physiology.

For tree crops, shortening the juvenile phase is a vital strategy to advance fruit bearing and enhance the breeding efficiency. Walnut (Juglans regia L.) seedlings usually take at least eight to 10 years to flower, but early-flowering (EF) types can flower one or two years after planting. In this study, RNA sequencing (RNA-Seq) and microRNA sequencing (miRNA-Seq) were used for a transcriptome-wide analysis of gene and miRNA expression in hybrids of the Xinjiang EF walnut variety 'Xinwen 81' and later-flowering (LF) walnut. Based on a high-quality chromosome-scale reference genome, a total of 3009 differentially expressed genes (DEGs) were identified, of which 933 were upregulated (accounting for 31%) and 2076 were downregulated (accounting for 69%). DEGs were functionally annotated, and the flowering-related genes FLOWERING LOCUS T (FT), SUPPRESSOR OF OVEREXPRESSION OF CO 1 (SOC1), and LEAFY (LFY) showed remarkable upregulation in EF compared with in the LF walnut. In addition, miRNAs associated with floral transition were screened as candidates for flowering time regulation in the walnut. This work provides new insights into walnut floral transition, which may ultimately contribute to genetic improvement of the walnut. [ABSTRACT FROM AUTHOR]