scholarly journals Transcriptomic profile analysis of mouse neural tube development by RNA-Seq

IUBMB Life ◽  
2017 ◽  
Vol 69 (9) ◽  
pp. 706-719 ◽  
Author(s):  
Juan Yu ◽  
Jianbing Mu ◽  
Qian Guo ◽  
Lihong Yang ◽  
Juan Zhang ◽  
...  
2020 ◽  
Author(s):  
Xinyue Li ◽  
Guangyu Ji ◽  
Juan Zhou ◽  
Jingyi Du ◽  
Xian Li ◽  
...  

Abstract Objective Early neural tube development in the embryo includes neural induction and self-renewal of neural stem cells (NSCs). The abnormal of neural tube development could lead to neural tube defects. The research on the mechanism of neural induction is the key to reveal the pathogenesis of the abnormal of neural tube. Though studies have confirmed a genetic component, the responsible mechanisms for the abnormal of neural tube are still largely unknown. Polycomb repressive complex 1 (PRC1) plays an important role in regulating early embryonic development, and has been sub-classified into six major complexes based on the presence of a Pcgf subunit. Pcgf1, as one of six Pcgf paralogs, is an important requirement in early embryonic brain development. Here, we intended to investigate the role and mechanism of Pcgf1 in early neural tube development of zebrafish embryos. Material and methods Morpholino (MO) antisense oligonucleotides were used to construct a Pcgf1 loss-of function zebrafish model. We analyzed the phenotype of zebrafish embryos and the expression of related genes in the process of neural induction by in situ hybridization, immunolabelling and RNA-sEq. The regulation of histone modifications on gene was detected by western blot and chromatin immunoprecipitation. Results In this study, we found that zebrafish embryos exhibited small head and reduced or even absence of telencephalon after inhibiting the expression of Pcgf1. Moreover, the neural induction process of zebrafish embryos was abnormal, and the subsequent NSCs self-renewal was inhibited under the inhibition of Pcgf1. RNA-seq and gene ontology (GO) analysis identified that the differentially expressed genes were enriched in many functional categories which related to the development phenotype. Finally, our results showed that Pcgf1 regulated the trimethylation of histone H3K27 in the Ngn1 and Otx2 promoter regions, and the levels of H3K4me3 at the promoters of Pou5f3 and Nanog. Conclusion Together, our data for the first time demonstrate that Pcgf1 plays an essential role in early neural induction phase through histone methylation in neural tube development. Our findings reveal a critical context-specific function for Pcgf1 in directing PRC1 to control cell fate.


2021 ◽  
Author(s):  
Ting Li ◽  
Quan Huo ◽  
Zhi Guo Lu ◽  
Xin Ran Xing ◽  
Lu Ding ◽  
...  

Abstract Background The occurrence of neural tube defects is a complex process in which genes, internal and external environment and other factors jointly influence and occur interactively. In this experiment, animal models of different energy balance states are constructed. To explore the mechanism of fos and leptin-leptin receptor during neural tube development of offspring under different energy states and its effect on neural tube development of offspringMethods Using gene identification technology to obtain Mex3c+/- negative energy balance mice and high-fat diet to obtain positive energy balance mice, and obtain E10.5d, E12.5d, E14.5d embryos. We will verify the expression of fos, leptin, LEPR, nestin, PAX3, and H3K27me3 proteins in the neural tube of the offspring through relevant experimental methods.Results We have successfully constructed animal models, Control group (18.82g±1.54g), Mex3c group (18.84g±1.08g), HFD group (22.61g±1.10g). Neural tube HE staining showen that compared with the Control group, the neuronal maturity of the Mex3c group and the HFD group was reduced. Immunohistochemical staining showed that both fos and leptin were expressed on the nucleus, and LEPR was expressed on the cell membrane. Western blot experiments showed that compared with the Control group, the Mex3c group and the HFD group had low expression of fos protein (P<0.01), the Mex3c group had high expression of LEPR protein (P<0.01) and the HFD group had high expression of LEPR protein (P<0.01). Immunostaining experiments showed that nestin was expressed in nerve fibers, and PAX3 and H3K27me3 were both expressed in the nucleus. Western blooting experiment showed that compared with the Control group, the Mex3c group had high expression of nestin protein (P<0.01), PAX3 protein (P<0.01), H3K27me3 (P<0.01), and the HFD group had high expression of nestin protein (P<0.01). ) And PAX3 protein (P<0.01), H3K27me3 (P<0.01).ConclusionsMex3c regulates leptin and LEPR by enhancing the expression of fos mRNA to participate in the neural tube development process of offspring. The neural tube nestin, PAX3, and H3K27me3 of the offspring of Mex3c+/- mice and high-fat diet mice continue to be highly expressed. Mex3c+/- mice express low leptin, and high-fat diet mice highly express leptin; preliminary reveals the regulation of different energy states Leptin-LEPR is involved in the process of neurodevelopment. Mex3c mutant mice and mice on a high-fat diet lead to decreased neurodevelopmental maturity.


Placenta ◽  
2017 ◽  
Vol 51 ◽  
pp. 118-119
Author(s):  
N. Santander ◽  
C. Lizama ◽  
A. Quiroz ◽  
A. Rigotti ◽  
D. Busso

2018 ◽  
Vol 34 (5) ◽  
pp. 933-938 ◽  
Author(s):  
Emrah Kantarcioglu ◽  
Gokmen Kahilogullari ◽  
Murat Zaimoglu ◽  
Esin Ozlem Atmis ◽  
Elif Peker ◽  
...  

Biomolecules ◽  
2019 ◽  
Vol 9 (4) ◽  
pp. 156 ◽  
Author(s):  
Wan-Long Su ◽  
Na Liu ◽  
Li Mei ◽  
Jie Luo ◽  
Yi-Jie Zhu ◽  
...  

To uncover the transcriptomic mechanism of lignin accumulation caused by boron deficiency (BD), Nanlin895 (Populus × euramericana “Nanlin895”) was subjected to control (CK, 0.25 mg·L−1) and BD (0 mg·L−1) treatments for 3 days. RNA-Seq was carried out to survey the expression patterns of the lignin-regulated biosynthetic genes in response to BD. The results showed that 5946 genes were identified as differentially expressed genes (DEGs), 2968 (44.2%) of which were upregulated and 3318 (55.8%) of which were downregulated in response to BD. Among them, the expression of lignin monomer biosynthetic (PAL, CCR, CAD, COMT, F5H, PER/LAC) and modulated genes, for example, transcription factors (MYBs) and hormone signal regulating genes (GIDs, histidine kinase 1, coronatine-insensitive protein 1), were upregulated, and some hormone signal regulating genes, such as AUXs and BR-related (sterol methyltransferases), were downregulated under BD treatment. There are also some genes that were screened as candidates for an association with wood formation, which will be used for the further analysis of the function of lignin formation. These results provide an important theoretical basis and reference data in plant for further research on the mechanism of lignin accumulation under BD.


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