Human Immunodeficiency Virus Type 1 Enhancer-binding Protein 3 Is Essential for the Expression of Asparagine-linked Glycosylation 2 in the Regulation of Osteoblast and Chondrocyte Differentiation

Imamura, Katsuyuki; Maeda, Shingo; Kawamura, Ichiro; Matsuyama, Kanehiro; Shinohara, Naoyuki; Yahiro, Yuhei; Nagano, Satoshi; Setoguchi, Takao; Yokouchi, Masahiro; Ishidou, Yasuhiro; Komiya, Setsuro

doi:10.1074/jbc.m113.520585

Cited by 19 publications

(14 citation statements)

References 43 publications

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“…The expression level of RUNX2 was similar in deformed and normal vertebrae, but conflicting results were obtained regarding RUNX2 regulation. Indeed, in deformed fish we observed a lower expression level of HIVEP3, a gene negatively regulating osteoblast differentiation by stimulating degradation of RUNX2 and acting as a damper for signalling pathways such as WNT, TGFβ and BMP2 [62][63][64][65][66]. TWIST2, a RUNX2 inhibitor, was up-regulated in deformed fish while activators, such as STAB2, were down-regulated [67].…”

Section: Resultsmentioning

confidence: 90%

RNA-Seq Transcriptome Analysis of Pronounced Biconcave Vertebrae: A Common Abnormality in Rainbow Trout (Oncorhynchus mykiss, Walbaum) Fed a Low-Phosphorus Diet

J¹,

MH²

2015

Next Generat Sequenc & Applic

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International audienceThe prevalence of bone deformities, particularly linked with mineral deficiency, is an important issue for fish production. Juvenile triploid rainbow trout (Oncorhynchus mykiss) were fed a low-phosphorus (P) diet for 27 weeks (60 to 630 g body mass). At study termination, 24.9% of the fish fed the low-P diet displayed homogeneous biconcave vertebrae (deformed vertebrae phenotype), while 5.5% displayed normal vertebral phenotypes for the entire experiment. The aim of our study was to characterize the deformed phenotype and identify the putative genes involved in the appearance of P deficiency-induced deformities. Both P status and biomechanical measurements showed that deformed vertebrae were significantly less mineralized (55.0 ± 0.4 and 59.4 ± 0.5,% ash DM, for deformed and normal vertebrae, respectively) resulting in a lower stiffness (80.3 ± 9.0 and 140.2 ± 6.3 N/mm, for deformed and normal phenotypes, respectively). The bone profiles based on μCT observations showed no difference in the osteoclastic resorption while no difference in matrix production was observed between deformed (total bone area 5442.0 ± 110.1 μm2) and normal vertebrae (total bone area 5931.2 ± 249.8 μm2) in this study. Consequently, the lower P content rather results from a reduced degree of mineralization in the deformed phenotype. Finally, we quantified differential gene expression between deformed vertebrae (pronounced biconcave) and normal phenotype by employing deep RNA-sequencing and mapping against a reference bone transcriptome for rainbow trout. In total, 1289 genes were differentially expressed. Among them, in deformed fish we observed that BGLAP, MGP and NOG, an inhibitor of BMP signalling pathway, were up-regulated while COL11a1 was down-regulated. These genes are central actors involved in the reduced degree of mineralization triggering vertebral deformities. These results will further the understanding of P deficiency-induced deformities; hence providing new tools for improved P management in production setting

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Section: Resultsmentioning

confidence: 90%

RNA-Seq Transcriptome Analysis of Pronounced Biconcave Vertebrae: A Common Abnormality in Rainbow Trout (Oncorhynchus mykiss, Walbaum) Fed a Low-Phosphorus Diet

J¹,

MH²

2015

Next Generat Sequenc & Applic

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“…Another gene that is up-regulated in the KO is the CCAAT/enhancer binding protein-β, cebp-b , a basic leucine zipper transcription factor that has been linked to endoplasmic reticulum mediated cell death (Meir et al, 2010) and is up-regulated in response to tBHQ (Hahn et al, 2014). A known Nfe2 target, human immunodeficiency virus type I enhancer binding protein 3b ( Hivep3b ) (Fujita et al, 2013), which is also a known regulator of endoplasmic stress (Imamura et al, 2014), was up-regulated in the KO at 2hpf upon pro-oxidant exposure. Thus, Nfe2 may be playing a role in suppressing factors that induce ER stress, perhaps in conjunction with Nrf2 (Cullinan et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

The transcription factor, Nuclear factor, erythroid 2 (Nfe2), is a regulator of the oxidative stress response during Danio rerio development

et al. 2016

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Development is a complex and well-defined process characterized by rapid cell proliferation and apoptosis. At this stage in life, a developmentally young organism is more sensitive to toxicants as compared to an adult. In response to pro-oxidant exposure, members of the Cap’n’Collar (CNC) basic leucine zipper (b-ZIP) transcription factor family (including Nfe2 and Nfe2-related factors, Nrfs) activate the expression of genes whose protein products contribute to reduced toxicity. Here, we studied the role of the CNC protein, Nfe2, in the developmental response to pro-oxidant exposure in the zebrafish (Danio rerio). Following acute waterborne exposures to diquat or tert-buytlhydroperoxide (tBOOH) at one of three developmental stages, wildtype (WT) and nfe2 knockout (KO) embryos and larvae were morphologically scored and their transcriptomes sequenced. Early in development, KO animals suffered from hypochromia that was made more severe through exposure to pro-oxidants; this phenotype in the KO may be linked to decreased expression of alas2, a gene involved in heme synthesis. WT and KO eleutheroembryos and larvae were phenotypically equally affected by exposure to pro-oxidants, where tBOOH caused more pronounced phenotypes as compared to diquat. Comparing diquat and tBOOH exposed embryos relative to the WT untreated control, a greater number of genes were up-regulated in the tBOOH condition as compared to diquat (tBOOH: 304 vs diquat: 148), including those commonly found to be differentially regulated in the vertebrate oxidative stress response (OSR) (e.g. hsp70.2, txn1, and gsr). When comparing WT and KO across all treatments and times, there were 1170 genes that were differentially expressed, of which 33 are known targets of the Nrf proteins Nrf1 and Nrf2. More specifically, in animals exposed to pro-oxidants a total of 968 genes were differentially expressed between WT and KO across developmental time, representing pathways involved in coagulation, embryonic organ development, body fluid level regulation, erythrocyte differentiation, and oxidation-reduction, amongst others. The greatest number of genes that changed in expression between WT and KO occurred in animals exposed to diquat at 2 h post fertilization (hpf). Across time and treatment, there were six genes (dhx40, cfap70, dnajb9b, slc35f4, spi-c, and gpr19) that were significantly up-regulated in KO compared to WT and four genes (fhad1, cyp4v7, nlrp12, and slc16a6a) that were significantly down-regulated. None of these genes have been previously identified as targets of Nfe2 or the Nrf family. These results demonstrate that the zebrafish Nfe2 may be a regulator of both primitive erythropoiesis and the OSR during development.

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“…Interestingly, the TFs ATF5 and CREB3L2 are described as transcriptional activators of differentiation processes of adipocytes (Zhao et al, 2014) and chondrocytes (Imamura et al, 2014;Saito et al, 2014), activating transcription by binding to the cAMP response element (Umemura et al, 2015). The TF ASB2 was identified as a growth inhibitor in myeloid leukemia cells (Guibal et al, 2002) through promoting ubiquitination of Notch targets such as E2A and JAK2 (Nie et al, 2011).…”

Section: Novel and Potentially Important Tfs For Th2 Cell Fate Decisionsmentioning

confidence: 99%

Data integration for identification of important transcription factors of STAT6-mediated cell fate decisions

et al. 2016

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ABSTRACT. Data integration has become a useful strategy for uncovering new insights into complex biological networks. We studied whether this approach can help to delineate the signal transducer and activator of transcription 6 (STAT6)-mediated transcriptional network driving T helper (Th) 2 cell fate decisions. To this end, we performed an integrative analysis of publicly available RNA-seq data of Stat6-knockout mouse studies together with STAT6 ChIP-seq data and our own gene expression time series data during Th2 cell differentiation. We focused on transcription factors (TFs), cytokines, and cytokine receptors and delineated 59 positively and 41 negatively STAT6-regulated genes, which were used to construct a transcriptional network around STAT6. The network illustrates that important and well-known TFs for Th2 cell differentiation are positively regulated by STAT6 and act either as activators for Th2 cells (e.g., Gata3, Atf3, Satb1, Nfil3, Maf, and Pparg) or as suppressors for other Th cell subpopulations such as Th1 (e.g., Ar), Th17 (e.g., Etv6), or iTreg (e.g., Stat3 and Hif1a) cells. Moreover, our approach reveals 11 TFs (e.g., Atf5, Creb3l2, and Asb2) with unknown functions in Th cell differentiation. This fact together with the observed enrichment of asthma risk genes among those regulated by STAT6 underlines the potential value of the data integration strategy used here. Thus, our results clearly support the opinion that data integration is a useful tool to delineate complex physiological processes.

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Human Immunodeficiency Virus Type 1 Enhancer-binding Protein 3 Is Essential for the Expression of Asparagine-linked Glycosylation 2 in the Regulation of Osteoblast and Chondrocyte Differentiation

Cited by 19 publications

References 43 publications

RNA-Seq Transcriptome Analysis of Pronounced Biconcave Vertebrae: A Common Abnormality in Rainbow Trout (Oncorhynchus mykiss, Walbaum) Fed a Low-Phosphorus Diet

RNA-Seq Transcriptome Analysis of Pronounced Biconcave Vertebrae: A Common Abnormality in Rainbow Trout (Oncorhynchus mykiss, Walbaum) Fed a Low-Phosphorus Diet

The transcription factor, Nuclear factor, erythroid 2 (Nfe2), is a regulator of the oxidative stress response during Danio rerio development

Data integration for identification of important transcription factors of STAT6-mediated cell fate decisions

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