Specific gene-regulation networks during the pre-implantation development of the pig embryo as revealed by deep sequencing

Cao, Suying; Wu, Jun; Li, Qiuyan; Liu, Zhong Hua; Zhang, Wei; Pei, Yangli; Ruan, Xiaoan; Wang, Xumin; Lim, Bing; Li, Ning

doi:10.1186/1471-2164-15-4

Cited by 124 publications

(162 citation statements)

References 54 publications

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“…1B). Consistent with the previous RNA sequencing data (Cao et al, 2014), RT-PCR results confirmed the absence of two other CDX family members, CDX1 and CDX4 (three technical replicates, Fig. S1C).…”

Section: Cdx2 Spatiotemporal Expression Pattern In Early-stage Porcinsupporting

confidence: 78%

CDX2 is essential for cell proliferation and polarity in porcine blastocysts

et al. 2017

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The role of CDX2 in trophectoderm (TE) cells has been extensively studied, yet the results are contradictory and species specific. Here, CDX2 expression and function were explored in early porcine embryos. Notably, siRNA-mediated gene knockdown and lentivirusmediated TE-specific gene regulation demonstrated that CDX2 is essential for the maintenance of blastocyst integrity by regulating the BMP4-mediated blastocyst niche and classic protein kinase C (PKC)-mediated TE polarity in mammalian embryos. Mechanistically, CDX2-depleted porcine embryos stalled at the blastocyst stage and exhibited apoptosis and inactive cell proliferation, possibly resulting from BMP4 downregulation. Moreover, TE cells in CDX2-depleted blastocysts displayed defective F-actin apical organization associated with downregulation of PKCα (PRKCA). Collectively, these results provide further insight into the functional diversity of CDX2 in early mammalian embryos.

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Section: Cdx2 Spatiotemporal Expression Pattern In Early-stage Porcinsupporting

confidence: 78%

CDX2 is essential for cell proliferation and polarity in porcine blastocysts

et al. 2017

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“…Before implantation, embryonic phenotypes for loss-offunction mutation of the pathway are not detected (20). Transcriptome sequencing and analyzing pig embryos in vivo and in vitro also show that the TGF␤ pathway is not active well before maternal zygotic transition at the four-to eight-cell stages (25). Those data suggest the function of the TGF␤ pathway is suppressed during early embryonic development.…”

Section: Discussionmentioning

confidence: 99%

RE1-silencing Transcription Factor (REST) Is Required for Nuclear Reprogramming by Inhibiting Transforming Growth Factor β Signaling Pathway

Kong

Xie

Zhang

et al. 2016

Journal of Biological Chemistry

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Edited by Eric R. FearonDifferentiated cells can be reprogrammed by transcription factors, and these factors that are responsible for successful reprogramming need to be further identified. Here, we show that the neuronal repressor RE1-silencing transcription factor (REST) is rich in porcine oocytes and requires for nuclear transfer (NT)-mediated reprogramming through inhibiting TGF␤ signaling pathway. REST was dramatically degraded after oocyte activation, but the residual REST was incorporated into the transferred donor nuclei during reprogramming in NT embryos. Inhibition of REST function in oocytes compromised the development of NT embryos but not that of IVF and PA embryos. Bioinformation analysis of putative targets of REST indicated that REST might function on reprogramming in NT embryos by inhibiting TGF␤ pathway. Further results showed that the developmental failure of REST-inhibited NT embryos could be rescued by treatment of SB431542, an inhibitor of TGF␤ pathway. Thus, REST is a newly discovered transcription factor that is required for NT-mediated nuclear reprogramming.Embryonic cells differentiate into all three germ layers of the body as development progresses. Once differentiated, the reversion of the differentiated state to pluripotency is strictly limited in normal development. However, experimentally the differentiated state can be returned to the pluripotent state by transcription factors (1, 2). Despite numerous attempts, the factors responsible for successful nuclear reprogramming still need to elucidate. Transcription factors maintaining the pluripotency of embryonic stem cells (ESCs) 3 are called pluripotent factors, and they have an important role in nuclear reprogramming, such as Oct4, Sox2, and Nanog (3, 4). Thus, we can identify and characterize reprogramming factors by screening the pluripotent factors. The repressor element 1 (RE1)-silencing transcription factor (REST), as a zinc finger protein, binds 21-bp RE1 sites and functions as a key negative regulator of neurogenesis, so it is also called neuron-restrictive silencer element (5). Recently, REST has been reported to induce gene expression by recruiting TET3 to the DNA for directed 5hmC generation and Nuclear SET domain-containing protein 3-mediated H3K36 trimethylation in neurons (6). Furthermore, REST has different roles in different cellular contexts, such as oncogenic and tumor-supressor functions and hematopoietic and cardiac differentiation (7,8). In 2008, REST was proved to maintain self-renewal and pluripotency of mouse ESCs through suppression of microRNAs and believed to be a major pluripotent factor (9, 10). However, it has not been elaborated in nuclear reprogramming. Here, we provide evidence that REST plays a unique role in NT-mediated reprogramming as a supressor of the TGF␤ signaling pathway in pig. ResultsExpression Pattern of REST-We first investigated the expression of REST in porcine oocytes, nuclear transfer (NT), and parthenogenetic activation (PA) embryos by real-time PCR and Western blotting analysis. P...

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“…After passing quality control, the RNA was treated and sequenced by the Novogene Bioinformation Institute as previously described (28). The RNAsequencing (RNA-Seq) data have been submitted to the National Center for Biotechnology Information Sequence Read archive (accession number: SRP052846, http://www.ncbi.nlm.nih.gov/sra).…”

Section: Rna Sequencingmentioning

confidence: 99%

Histone Arginine Methylation by PRMT7 Controls Germinal Center Formation via Regulating Bcl6 Transcription

Ying

Mei

Zhang

et al. 2015

The Journal of Immunology

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B cells are the center of humoral immunity and produce Abs to protect against foreign Ags. B cell defects lead to diseases such as leukemia and lymphomas. Histone arginine methylation is important for regulating gene activation and silencing in cells. Although the process commonly exists in mammalian cells, its roles in B cells are unknown. To explore the effects of aberrant histone arginine methylation on B cells, we generated mice with a B cell–specific knockout of PRMT7, a member of the methyltransferases that mediate arginine methylation of histones. In this article, we showed that the loss of PRMT7 led to decreased mature marginal zone B cells and increased follicular B cells and promoted germinal center formation after immunization. Furthermore, mice lacking PRMT7 expression in B cells secreted low levels of IgG1 and IgA. Abnormal expression of germinal center genes (i.e., Bcl6, Prdm1, and Irf4) was detected in conditional knockout mice. By overexpressing PRMT7 in the Raji and A20 cell lines derived from B cell lymphomas, we validated the fact that PRMT7 negatively regulated Bcl6 expression. Using chromatin immunoprecipitation–PCR, we found that PRMT7 could recruit H4R3me1 and symmetric H4R3me2 to the Bcl6 promoter. These results provide evidence for the important roles played by PRMT7 in germinal center formation.

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Specific gene-regulation networks during the pre-implantation development of the pig embryo as revealed by deep sequencing

Cited by 124 publications

References 54 publications

CDX2 is essential for cell proliferation and polarity in porcine blastocysts

CDX2 is essential for cell proliferation and polarity in porcine blastocysts

RE1-silencing Transcription Factor (REST) Is Required for Nuclear Reprogramming by Inhibiting Transforming Growth Factor β Signaling Pathway

Histone Arginine Methylation by PRMT7 Controls Germinal Center Formation via Regulating Bcl6 Transcription

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