Analysis of the role of lncRNA in reprogramming in Guangzhou Institute of Biology

Analysis of the role of lncRNA in reprogramming in Guangzhou Institute of Biology

On December 16, 2014, researchers from the Guangzhou Institute of Biomedicine and Health, Chinese Academy of Sciences, Shandong University, Southern Medical University, Birmingham University and the University of Hong Kong published a new research in the internationally renowned academic journal Cell Research. , entitled "The p53-induced lincRNA-p21 derails somatic cell reprogramming by sustaining H3K9me3 and CpG methylation at pluripotency gene promoters". This study provides unique insights into the role of lncRNAs in reprogramming and establishes a new link between p53 and heterochromatin.

The authors of this article are Miguel A. Esteban, a Hispanic researcher at the Guangzhou Institute of Biomedicine and Health, Chinese Academy of Sciences, and Dr. Bao Xiyu, an associate researcher. Dr. Miguel A. Esteban graduated from the Autonomous University of Madrid, Spain. He has worked in Navarra University and Imperial College London. In December 2007, he joined the Guangzhou Institute of Biomedicine and Health, where he worked on cancer stem cell research. Published in the international authoritative journals such as Cell stem cell, JBC, Nature Genetics, Human Molecular genetic. Dr. Bao Xiyu received his Ph.D. degree in Chinese University of Science and Technology in Biochemistry and Molecular Biology in 2011. He has been an assistant researcher and associate researcher at the Guangzhou Institute of Biomedicine and Health since 2011. He is mainly engaged in the function of non-coding RNA in the induction of pluripotent stem cells. He has published academic papers in famous journals such as JBC, Current Opinion in Cell Biology, and Nucleic Acid Research.

Induced pluripotent stem cells (iPSCs) have important implications for regenerative medicine, in vitro disease models, and toxicological screening. However, to achieve these expectations, it is necessary to understand how the reprogramming mechanism eliminates and rewrites somatic epigenetic coding. This is important because reprogramming is prone to errors, which can hinder biomedical applications of derived cells.

Now, reprogramming by exogenous factors is considered a multi-step process in which cells must overcome a series of obstacles in order to obtain pluripotency, but in some cases it may also be deterministic. . Two basic reprogramming hurdles are: p53-mediated responses that promote apoptosis and cellular senescence; the removal of pre-existing somatic-like epigenetic markers is inefficient. Therefore, the loss of p53 or H3K9 methyltransferases Setdb1, Suv39h1 and Suv39h2, as well as the inhibition of DNA methyltransferase DNMT1, can increase the efficiency of reprogramming.

Non-coding RNAs play an important role in the construction or deletion of different reprogramming disorders. However, despite the extensive characterization of microRNA (miRNA) networks in reprogramming, only two long non-coding RNAs (lncRNAs) are known to modulate this process. LncRNAs are non-coding RNA species of up to 200 nucleotides that act as baits, guides or scaffolds. LincRNA-RoR is the first lncRNA involved in reprogramming. In contrast, lincRNA TUNA forms several complexes with several RNA-binding proteins of the Nanog, Sox2 and Fgf4 promoter regions, where it facilitates the deposition of the active histone marker H3K4me3.

In this study, by expression profiling and functional screening, the researchers determined that large intergenic non-coding RNA p21 (lincRNA-p21) can impair reprogramming. Notably, lincRNA-p21 is induced by p53 but does not promote apoptosis or cellular senescence in reprogramming. In contrast, lincRNA-p21 is involved in the H3K9 methyltransferase SETDB1 and the DNA methyltransferase DNMT1, which is promoted by the RNA binding protein HNRNPK. Thus, lincRNA-p21 can prevent reprogramming by maintaining H3K9me3 and/or CpG methylation of the pluripotency gene promoter.

In the process of this paper, Dimitrova et al. used a gene deletion method to demonstrate that lincRNA-p21 also acts cis to induce p21 expression and reduce MEF proliferation. In contrast to our work, Huarte et al. did not detect any reduction in p21 expression after knocking out lincRNA-p21 of MEFs. Dimitrova et al. also speculated that lincRNA-p21 blocked OSKM reprogramming of MEFs by increasing p21, but they did not quantify cell proliferation in this setting. One possible explanation for this difference is that complete inhibition of lincRNA-p21 is required for the release of p21. Further experiments are needed to clarify this issue, and it is possible that lincRNA-p21 regulates reprogramming through a variety of mechanisms.

In conclusion, this study can guide other researchers to investigate the role of lncRNA in reprogramming, and also point to a new mechanism by which p53, HNRNPK and lincRNA-p21 regulate gene expression. Future research will further explore the network controlled by lincRNA during reprogramming, which will form new links with the obstacles identified so far.

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