scholarly journals Epigenetic regulation of gene expression in porcine epiblast, hypoblast, trophectoderm and epiblast-derived neural progenitor cells

Epigenetics ◽  
2011 ◽  
Vol 6 (9) ◽  
pp. 1149-1161 ◽  
Author(s):  
Yu Gao ◽  
Helene Jammes ◽  
Mikkel Aabech Rasmussen ◽  
Olga Oestrup ◽  
Nathalie Beaujean ◽  
...  
2009 ◽  
Vol 87 (14) ◽  
pp. 3143-3152 ◽  
Author(s):  
Randal X. Moldrich ◽  
Luce Dauphinot ◽  
Julien Laffaire ◽  
Tania Vitalis ◽  
Yann Hérault ◽  
...  

Gene Therapy ◽  
2008 ◽  
Vol 16 (3) ◽  
pp. 349-358 ◽  
Author(s):  
I Rothenaigner ◽  
S Kramer ◽  
M Meggendorfer ◽  
A Rethwilm ◽  
R Brack-Werner

2014 ◽  
Vol 34 (27) ◽  
pp. 9107-9123 ◽  
Author(s):  
A. Somasundaram ◽  
A. K. Shum ◽  
H. J. McBride ◽  
J. A. Kessler ◽  
S. Feske ◽  
...  

2021 ◽  
Author(s):  
Belkis Atasever Arslan ◽  
Scott T. Brady ◽  
Gamze Gunal Sadik

Transcriptional regulation of protein-coding genes is a primary control mechanism of cellular function. Similarities in regulation of expression for select genes between lymphocytes and neurons have led to proposals that such genes may be useful biomarkers for some neurological disorders that can be monitored via patient lymphocyte populations. Examination of shared molecular mechanisms underlying neurogenesis and lymphocyte differentiation may give help to identify relevant pathways and suggest additional biomarkers in lymphocytes that are relevant to neurological disorders. In this study, we analysed similarities and conserved regions in several genes regulated by CCCTC-binding factor (CTCF) during lymphocyte and neuronal developmental stages. We performed epigenetic analysis of CTCF binding Trak1, Gabpa, Gabpb1, Gabpb2, Gfi1, Gfi1b gene loci at T and B lymphocytes at different developmental stages, as well as in neural progenitor cells and motor neurons. Common and shared CTCF binding events at Trak1 gene suggest additional transcriptional regulatory factors that control Trak1 gene expression levels differ in neurons and lymphocytes. Gabpb1 gene includes a common CTCF binding site shared with neurons and lymphocytes. Correlation of CTCF binding analysis and gene expression profile suggests that CTCF binding plays a role in epigenetic regulation of Gabpb1 gene. In contrast, while Gfi1a gene is phylogenetically well-conserved and CTCF sites are occupied in lymphocytes, there are no CTCF binding occupied in neurons and neural progenitor cells. Low expression levels of Gfi1s in neurons indicate that regulation of this gene is CTCF-independent in neurons. Although Gfi1b is highly homologous to Gfi1, differences in expression levels suggest that Gfi1b is critical for both lymphogenesis and neurogenesis. Neurons and lymphocytes have multiple common CTCF binding sites in the Gfi1b gene, although lineage specific transcriptional regulators that play a role in their different expression levels still need to be identified. The partial overlap in CTCF regulatory sites for some genes in neurons and lymphocytes suggest that there may be markers that can exhibit parallel changes in these cells and serve as biomarkers.


2021 ◽  
Author(s):  
Benjamin Shea O'Brien ◽  
Rebekah L Mokry ◽  
Megan L Schumacher ◽  
Kirthi Pulakanti ◽  
Sridhar Rao ◽  
...  

Human cytomegalovirus (HCMV) is a beta herpesvirus that, upon congenital infection, can cause severe birth defects including vision and hearing loss, microcephaly, and seizures. Currently, no approved treatment options exist for in utero infections. We previously demonstrated that HCMV infection decreases calcium signaling responses and alters neuronal differentiation in induced pluripotent stem cell (iPSC) derived neural progenitor cells (NPCs). Here we aimed to determine the impact of infection on the transcriptome in developing human neurons using iPSC-derived 3-dimensional cerebral organoids. We infected iPSC-derived cerebral organoids with HCMV encoding eGFP and sorted cell populations based on GFP signal strength. Significant transcriptional downregulation was observed including in key neurodevelopmental gene pathways in both the GFP (+) and intermediate groups. Interestingly, the GFP (-) group also showed downregulation of the same targets indicating a mismatch between GFP expression and viral infection. Using a modified HCMV virus destabilizing IE 1 and 2 proteins, we still observed significant downregulation of neurodevelopmental gene expression in infected neural progenitor cells. Together, these data indicate that IE viral proteins are not the main drivers of neurodevelopmental gene dysregulation in HCMV infected neural tissues suggesting therapeutically targeting IE gene expression is insufficient to restore neural differentiation and function.


Sign in / Sign up

Export Citation Format

Share Document