BackgroundPhenolic aldehydes generated from lignocellulose pretreatment exhibited severe toxic inhibitions on microbial growth and fermentation. Numerous tolerance studies against furfural, 5-hydroxymethyl-2-furaldehyde (HMF), acetate, and ethanol were reported, but studies on inhibition of phenolic aldehyde inhibitors are rare. For ethanologenic strains, Zymomonas mobilis ZM4 is high in ethanol productivity and genetic manipulation feasibility, but sensitive to phenolic aldehyde inhibitors. Molecular mechanisms of tolerance for Z. mobilis toward phenolic aldehydes are not known.ResultsWe took the first insight into genomic response of Z. mobilis ZM4 to the phenolic aldehyde inhibitors derived from lignocellulose pretreatment. The results suggest that the toxicity to cells is caused by the functional group of phenolic aldehyde, similar to furfural and HMF, rather than aromatic groups or phenolic hydroxyl groups. Transcriptome response against 4-hydroxybenzaldehyde, syringaldehyde, and vanillin, representing phenolic groups H, S, and G, respectively, was investigated. The atlas of the important genes responsible for significantly enhanced and repressed genes at the genomic level was illustrated. 272 genes with twofold greater expressions than non-treated controls and 36 gene clusters in response to challenges of these phenolic aldehydes were identified. Several reductases encoded by ZMO1116, ZMO1696, and ZMO1885 were found to play the key roles in reducing phenolic aldehydes into the corresponding phenolic alcohols. Reduction of phenolic aldehydes by overexpression of ZMO1116, ZMO1696, and ZMO1885 in Z. mobilis ZM4 resulted in the increased inhibitor conversion and ethanol productivity, especially for 4-hydroxybenzaldehyde and vanillin. Several transporter genes such as ZMO0282, ZMO0283, ZMO0798, ZMO0799, and ZMO0800 was also displayed significantly increased expressions against the phenolic aldehydes.ConclusionsThe genes encoding reductases are with potentials on phenolic aldehydes-tolerant genes contributing to the reduction of phenolic aldehydes into the corresponding phenolic alcohols forms for Z. mobilis ZM4. Overexpression of the key genes improved the conversion ratio and ethanol productivity of 4-hydroxybenzaldehyde and vanillin with high toxicity. New knowledge obtained from this research aids understanding the mechanisms of bacterial tolerance and the development of the next-generation biocatalysts for advanced biofuels production.Electronic supplementary materialThe online version of this article (doi:10.1186/s13068-015-0333-9) contains supplementary material, which is available to authorized users.

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Adipogenesis, a physiological process initiated with the committed preadipocytes expressing adipocyte-specific genes and terminated in mature, differentiated and functional adipocytes, mainly involved with energy homeostasis. Abnormal distributionchanges and dysfunctions in adipogenesis may lead to complex physiopathological disorders. However, it remains unclear for the key players working for the whole complex differentiating process of adipogenesis. Here, it investigated transcriptional profiling of adipogenesis from human mesenchymal stem cells (hMSCs) by RNA-Seq transcriptome technique. Oil Red O staining assays were performed to assess adipogenic potential.Quantitative real-time PCR (qRT-PCR) and lentivirus transfection assays by small interference RNA (siRNA) were conducted to confirm the function of the candidate genes. A total of 1,078 differentially expressed genes shared at 7, 14, 21, and 28 days during adipogenesis from hMSCs, and 706 genes were significantly differentially expressed. It identified 20 potential key genes responsible for adipogenesis with four genes downregulating. The candidate gene, coagulation factor II thrombin receptor (F2R), encoding coagulation factor II thrombin receptor involving with a 7-transmembrane receptor involved in the regulation of thrombotic response, also known as proteinaseactivated receptor-1, contributed to adipogenesis, especially at Day 14, by Oil Red O staining, qRT-PCR, and western blot after siRNA. A unique discovery shed new light to understand the key players of the whole processes of adipogenesis from hMSCs. The gene F2R might be used as an adipogenic marker to provide a potential target for understanding the metabolic syndromes like obesity, type-2 diabetes, steatosis, atherosclerosis, and osteoporosis.

Background Fast, complete, and ultimate removal of inhibitory compounds derived from lignocellulose pretreatment is the prerequisite for efficient production of cellulosic ethanol and biochemicals. Biodetoxification is the most promising method for inhibitor removal by its unique advantages. The biodetoxification mechanisms of a unique diploid fungus responsible for highly efficient biodetoxification in solid-state culture was extensively investigated in the aspects of cellular structure, genome sequencing, transcriptome analysis, and practical biodetoxification. Results The inborn heterozygous diploid structure of A. resinae ZN1 uniquely contributed to the enhancement of inhibitor tolerance and conversion. The co-expression of gene pairs contributed to the enhancement of the degradation of lignocellulose-derived model inhibitors. The ultimate inhibitors degradation pathways and sugar conservation were elucidated by microbial degradation experimentation as well as the genomic and transcriptomic sequencing analysis. Conclusions The finding of the heterozygous diploid structure in A. resinae ZN1 on biodetoxification took the first insight into the global overview of biodetoxification mechanism of lignocellulose-derived inhibitors. This study provided a unique and practical biodetoxification biocatalyst of inhibitor compounds for lignocellulose biorefinery processing, as well as the synthetic biology tools on biodetoxification of biorefinery fermenting strains. Electronic supplementary material The online version of this article (10.1186/s13068-019-1466-z) contains supplementary material, which is available to authorized users.