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ABSTRACTOur understanding of adipose tissue has progressed from an inert tissue for energy storage to be one of the largest endocrine organs regulating metabolic homoeostasis through its ability to synthesize and release various adipokines that regulate a myriad of pathways. The field of adipose tissue biology is growing due to this association with various chronic metabolic diseases. An important process in the regulation of adipose tissue biology is adipogenesis, which is the formation of new adipocytes. Investigating adipogenesis in vitro is currently a focus for identifying factors that might be utilized in clinically. A powerful tool for such work is high-throughput sequencing which can rapidly identify changes at gene expression level. Various cell models exist for studying adipogenesis and has been used in high-throughput studies, yet little is known about transcriptome profile that underlies adipogenesis in mouse embryonic fibroblasts. This study utilizes RNA-sequencing and computational analysis with DESeq2, gene ontology, protein–protein networks, and robust rank analysis to understand adipogenesis in mouse embryonic fibroblasts in-depth. Our analyses confirmed the requirement of mitotic clonal expansion prior to adipogenesis in this cell model and highlight the role of Cebpa and Cebpb in regulating adipogenesis through interactions of large numbers of genes.

•Aberrant expression patterns of miRNAs are reported in prostate cancer and are triggered by multiple genomic anomalies.•Dysregulated miRNAs are proved to contribute to prostate tumorigenesis by modulating crucial carcinogenic processes.•High-throughput methods are exploited to profile miRNAs in prostate cancer patients.•miRNAs’ unique properties make them convenient tools as biomarkers for prostate cancer diagnosis, prognosis, and therapy response assessment.•miRNAs-based therapeutics are promising tools to reverse the pathological alterations of miRNAs and manage prostate cancer.

Direct cell programming via overexpression of transcription factors (TFs) aims to control cell fate with the degree of precision needed for clinical applications. However, the regulatory steps involved in successful terminal cell fate programming remain obscure. We have investigated the underlying mechanisms by looking at gene expression, chromatin states, and TF binding during the uniquely efficient Ngn2, Isl1, and Lhx3 motor neuron programming pathway. Our analysis reveals a highly dynamic process in which Ngn2 and the Isl1/Lhx3 pair initially engage distinct regulatory regions. Subsequently, Isl1/Lhx3 binding shifts from one set of targets to another, controlling regulatory region activity and gene expression as cell differentiation progresses. Binding of Isl1/Lhx3 to later motor neuron enhancers depends on the Ebf and Onecut TFs, which are induced by Ngn2 during the programming process. Thus, motor neuron programming is the product of two initially independent transcriptional modules that converge with a feedforward transcriptional logic.