HNF factors form a network to regulate liver-enriched genes in zebrafish

Wei, Cheng; Guo, Lin; Zhang, Zhenhai; Soo, Hui Meng; Wen, Chuangyu; Wu, Wei; Peng, Jinrong

doi:10.1016/j.ydbio.2006.03.018

Cited by 82 publications

(67 citation statements)

References 46 publications

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“…As a second example, the top 10 TF predictors of liver expression included Hepatocyte Nuclear Factor 1 (TCF1), HNF4A, PPARA, SREBF1, HNF4-DR1, NR2F2, and NR1H4 ( Fig. 4A), all of which are known regulatory proteins important in liver function (Shih et al 2001;Zannis et al 2001;Cheng et al 2006). These two examples highlight the biological plausibility of the EI method to predict tissue-specific gene expression.…”

Section: Determining Sequence Signatures Of Candidate Tissue-specificmentioning

confidence: 96%

Predicting tissue-specific enhancers in the human genome

Pennacchio¹,

Loots²,

Nóbrega³

et al. 2007

Genome Res.

124

131

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Determining how transcriptional regulatory signals are encoded in vertebrate genomes is essential for understanding the origins of multicellular complexity; yet the genetic code of vertebrate gene regulation remains poorly understood. In an attempt to elucidate this code, we synergistically combined genome-wide gene-expression profiling, vertebrate genome comparisons, and transcription factor binding-site analysis to define sequence signatures characteristic of candidate tissue-specific enhancers in the human genome. We applied this strategy to microarray-based gene expression profiles from 79 human tissues and identified 7187 candidate enhancers that defined their flanking gene expression, the majority of which were located outside of known promoters. We cross-validated this method for its ability to de novo predict tissue-specific gene expression and confirmed its reliability in 57 of the 79 available human tissues, with an average precision in enhancer recognition ranging from 32% to 63% and a sensitivity of 47%. We used the sequence signatures identified by this approach to successfully assign tissue-specific predictions to ∼328,000 human-mouse conserved noncoding elements in the human genome. By overlapping these genome-wide predictions with a data set of enhancers validated in vivo, in transgenic mice, we were able to confirm our results with a 28% sensitivity and 50% precision. These results indicate the power of combining complementary genomic data sets as an initial computational foray into a global view of tissue-specific gene regulation in vertebrates.

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Section: Determining Sequence Signatures Of Candidate Tissue-specificmentioning

confidence: 96%

Predicting tissue-specific enhancers in the human genome

Pennacchio¹,

Loots²,

Nóbrega³

et al. 2007

Genome Res.

124

131

View full text Add to dashboard Cite

show abstract

“…The gfp probe was amplified from the gfp gene using primer pair EGFP-U322 and EGFP-L742 (Supplemental Table S1). Digoxigenin (DIG)-labeled probes were used in Northern blot hybridization as described (Cheng et al 2006). Primer pairs used in RT-qPCR for detecting D113p53 and el1a were as described previously (Chen et al 2005).…”

Section: Rna and Protein Analysis Rt-pcrmentioning

confidence: 99%

p53 isoform Δ113p53 is a p53 target gene that antagonizes p53 apoptotic activity via BclxL activation in zebrafish

Chen¹,

Ng²,

Chang³

et al. 2009

Genes Dev.

Self Cite

145

197

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p53 is a well-known tumor suppressor and is also involved in processes of organismal aging and developmental control. A recent exciting development in the p53 field is the discovery of various p53 isoforms. One p53 isoform is human D133p53 and its zebrafish counterpart D113p53. These N-terminal-truncated p53 isoforms are initiated from an alternative p53 promoter, but their expression regulation and physiological significance at the organismal level are not well understood. We show here that zebrafish D113p53 is directly transactivated by full-length p53 in response to developmental and DNA-damaging signals. More importantly, we show that D113p53 functions to antagonize p53-induced apoptosis via activating bcl2L (closest to human Bcl-x L ), and knockdown of D113p53 enhances p53-mediated apoptosis under stress conditions. Thus, we demonstrate that the p53 genetic locus contains a new p53 response gene and that D113p53 does not act in a dominant-negative manner toward p53 but differentially modulates p53 target gene expression to antagonize p53 apoptotic activity at the physiological level in zebrafish. Our results establish a novel feedback pathway that modulates the p53 response and suggest that modulation of the p53 pathway by p53 isoforms might have an impact on p53 tumor suppressor activity.[Keywords: p53 isoforms; D113p53; Bcl2; apoptosis; zebrafish] Supplemental material is available at http://www.genesdev.org.

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“…9,10 The liver, a main target for nanomaterial toxicity, is an essential organ that plays a number of vital functions including processing nutrients from ingested food, maintaining metabolites in the blood, and serving as a site for detoxification. 11 The bloodbrain barrier (BBB) is a highly selective permeability barrier that separates circulating blood from brain extracellular fluid in the central nervous system (CNS). The BBB allows the passage of water, some gases, and lipid-soluble molecules by passive diffusion, as well as the selective transport of molecules such as glucose and amino acids that are crucial to neural functions.…”

Section: Introductionmentioning

confidence: 99%

Effects of copper oxide nanoparticles on developing zebrafish embryos and larvae

Zhang¹,

He²,

Wang³

et al. 2016

IJN

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Copper oxide nanoparticles (CuO NPs) are used for a variety of purposes in a wide range of commercially available products. Some CuO NPs probably end up in the aquatic systems, thus raising concerns about aqueous exposure toxicity, and the impact of CuO NPs on liver development and neuronal differentiation remains unclear. In this study, particles were characterized using Fourier transform infrared spectra, scanning electron microscopy, and transmission electron microscopy. Zebrafish embryos were continuously exposed to CuO NPs from 4 hours postfertilization at concentrations of 50, 25, 12.5, 6.25, or 1 mg/L. The expression of gstp1 and cyp1a was examined by quantitative reverse transcription polymerase chain reaction. The expression of tumor necrosis factor alpha and superoxide dismutase 1 was examined by quantitative reverse transcription polymerase chain reaction and Western blotting. Liver development and retinal neurodifferentiation were analyzed by whole-mount in situ hybridization, hematoxylin–eosin staining, and immunohistochemistry, and a behavioral test was performed to track the movement of larvae. We show that exposure of CuO NPs at low doses has little effect on embryonic development. However, exposure to CuO NPs at concentrations of 12.5 mg/L or higher leads to abnormal phenotypes and induces an inflammatory response in a dose-dependent pattern. Moreover, exposure to CuO NPs at high doses results in an underdeveloped liver and a delay in retinal neurodifferentiation accompanied by reduced locomotor ability. Our data demonstrate that short-term exposure to CuO NPs at high doses shows hepatotoxicity and neurotoxicity in zebrafish embryos and larvae.

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HNF factors form a network to regulate liver-enriched genes in zebrafish

Cited by 82 publications

References 46 publications

Predicting tissue-specific enhancers in the human genome

Predicting tissue-specific enhancers in the human genome

p53 isoform Δ113p53 is a p53 target gene that antagonizes p53 apoptotic activity via BclxL activation in zebrafish

Effects of copper oxide nanoparticles on developing zebrafish embryos and larvae

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