The development and transcriptome regulation of the secondary trunk of Ginkgo biloba L.

Secondary trunk Ginkgo biloba is one of the specific germplasms of G. biloba. In this study, paraffin sectioning, high-performance liquid chromatography and transcriptome sequencing technology were used to study the development of the secondary trunk of G. biloba from the morphological, physiological and molecular levels. The results showed that the secondary trunk of G. biloba originated from the latent buds in the stem cortex at the junction of the root and stem of the main trunk. The development process of secondary trunk was divided into 4 periods: the dormancy period of the secondary trunk buds, the differentiation period, the formation period of transport tissue, and the budding period. Transcriptome sequencing was performed by comparing the germination period and elongation growth period of the secondary trunk with the normal parts of the same period where no secondary trunks occurred. Differential genes involved in phytohormone signal transduction, phenylpropane biosynthesis, phenylalanine metabolism, glycolysis and other pathways can regulate not only the inhibition of early dormant buds but also the later development of the secondary trunk. Genes related to IAA synthesis are upregulated and indole-3-acetic acid content is increased, leading to the up-regulated expression of IAA intracellular vector genes. The IAA response gene (SAUR) receives and responds to IAA signals to promote the development of the secondary trunk. Through the enrichment of differential genes and functional annotations, a key regulatory pathway map for the occurrence of the secondary trunk of G. biloba was sorted out.

Network analysis of microRNAs, transcription factors, and target genes involved in axon regeneration.

Axon regeneration is crucial for recovery from neurological diseases. Numerous studies have identified several genes, microRNAs (miRNAs), and transcription factors (TFs) that influence axon regeneration. However, the regulatory networks involved have not been fully elucidated. In the present study, we analyzed a regulatory network of 51 miRNAs, 27 TFs, and 59 target genes, which is involved in axon regeneration. We identified 359 pairs of feed-forward loops (FFLs), seven important genes (Nap1l1, Arhgef12, Sema6d, Akt3, Trim2, Rab11fip2, and Rps6ka3), six important miRNAs (hsa-miR-204-5p, hsa-miR-124-3p, hsa-miR-26a-5p, hsa-miR-16-5p, hsa-miR-17-5p, and hsa-miR-15b-5p), and eight important TFs (Smada2, Fli1, Wt1, Sp6, Sp3, Smad4, Smad5, and Creb1), which appear to play an important role in axon regeneration. Functional enrichment analysis revealed that axon-associated genes are involved mainly in the regulation of cellular component organization, axonogenesis, and cell morphogenesis during neuronal differentiation. However, these findings need to be validated by further studies.

Network analysis identifies common genes associated with obesity in six obesity-related diseases.

Obesity has been reported to be associated with many diseases. However, common obesity-induced biological processes have not been evaluated across these diseases. We identified genes associated with obesity and obesity-related diseases, and used them to construct protein‒protein interaction networks. We also analyzed gene ontology (GO) in those genes overlapping between obesity and disease. Our work identifies gene modules common to obesity and obesity-related diseases, which can provide a basis for understanding the process of how obesity induces disease.

Identification of neuron-related genes for cell therapy of neurological disorders by network analysis.

Bone mesenchymal stem cells (BMSCs) differentiated into neurons have been widely proposed for use in cell therapy of many neurological disorders. It is therefore important to understand the molecular mechanisms underlying this differentiation. We screened differentially expressed genes between immature neural tissues and untreated BMSCs to identify the genes responsible for neuronal differentiation from BMSCs. GSE68243 gene microarray data of rat BMSCs and GSE18860 gene microarray data of rat neurons were received from the Gene Expression Omnibus database. Transcriptome Analysis Console software showed that 1248 genes were up-regulated and 1273 were down-regulated in neurons compared with BMSCs. Gene Ontology functional enrichment, protein-protein interaction networks, functional modules, and hub genes were analyzed using DAVID, STRING 10, BiNGO tool, and Network Analyzer software, revealing that nine hub genes, Nrcam, Sema3a, Mapk8, Dlg4, Slit1, Creb1, Ntrk2, Cntn2, and Pax6, may play a pivotal role in neuronal differentiation from BMSCs. Seven genes, Dcx, Nrcam, sema3a, Cntn2, Slit1, Ephb1, and Pax6, were shown to be hub nodes within the neuronal development network, while six genes, Fgf2, Tgfß1, Vegfa, Serpine1, Il6, and Stat1, appeared to play an important role in suppressing neuronal differentiation. However, additional studies are required to confirm these results.