The Evolution of Gene Regulatory Mechanisms in Bacteria

Author(s):  
Charles J. Dorman ◽  
Niamh Ní Bhriain ◽  
Matthew J. Dorman
Author(s):  
Lei Guan ◽  
Ting Li ◽  
Nanping Ai ◽  
Wei Wang ◽  
Bing He ◽  
...  

Abstract Background MEIS2 has been identified as one of the key transcription factors in the gene regulatory network in the development and pathogenesis of human cancers. Our study aims to identify the regulatory mechanisms of MEIS2 in hepatocellular carcinoma (HCC), which could be targeted to develop new therapeutic strategies. Methods The variation of MEIS2 levels were assayed in a cohort of HCC patients. The proliferation, clone-formation, migration, and invasion abilities of HCC cells were measured to analyze the effects of MEIS2C and MEIS2D (MEIS2C/D) knockdown with small hairpin RNAs in vitro and in vivo. Chromatin immunoprecipitation (ChIP) was performed to identify MEIS2 binding site. Immunoprecipitation and immunofluorescence assays were employed to detect proteins regulated by MEIS2. Results The expression of MEIS2C/D was increased in the HCC specimens when compared with the adjacent noncancerous liver (ANL) tissues. Moreover, MEIS2C/D expression negatively correlated with the prognosis of HCC patients. On the other hand, knockdown of MEIS2C/D could inhibit proliferation and diminish migration and invasion of hepatoma cells in vitro and in vivo. Mechanistically, MESI2C activated Wnt/β-catenin pathway in cooperation with Parafibromin (CDC73), while MEIS2D suppressed Hippo pathway by promoting YAP nuclear translocation via miR-1307-3p/LATS1 axis. Notably, CDC73 could directly either interact with MEIS2C/β-catenin or MEIS2D/YAP complex, depending on its tyrosine-phosphorylation status. Conclusions Our studies indicate that MEISC/D promote HCC development via Wnt/β-catenin and Hippo/YAP signaling pathways, highlighting the complex molecular network of MEIS2C/D in HCC pathogenesis. These results suggest that MEISC/D may serve as a potential novel therapeutic target for HCC.


2016 ◽  
Vol 48 (4) ◽  
pp. 387-397 ◽  
Author(s):  
Thomas Whitington ◽  
Ping Gao ◽  
Wei Song ◽  
Helen Ross-Adams ◽  
Alastair D Lamb ◽  
...  

PLoS Genetics ◽  
2015 ◽  
Vol 11 (12) ◽  
pp. e1005754 ◽  
Author(s):  
Anthony J. E. Berndt ◽  
Jonathan C. Y. Tang ◽  
Marc S. Ridyard ◽  
Tianshun Lian ◽  
Kathleen Keatings ◽  
...  

2009 ◽  
Vol 284 (46) ◽  
pp. 32002-32014 ◽  
Author(s):  
Yukiko Noguchi ◽  
Takahiro Hirabayashi ◽  
Shota Katori ◽  
Yoshimi Kawamura ◽  
Makoto Sanbo ◽  
...  

2004 ◽  
Vol 15 (2) ◽  
pp. 303-313 ◽  
Author(s):  
José Garcı́a-Martı́nez ◽  
Agustı́n Aranda ◽  
José E Pérez-Ortı́n

2018 ◽  
Author(s):  
Asija Diag ◽  
Marcel Schilling ◽  
Filippos Klironomos ◽  
Salah Ayoub ◽  
Nikolaus Rajewsky

SUMMARYIn animal germlines, regulation of cell proliferation and differentiation is particularly important but poorly understood. Here, using a cryo-cut approach, we mapped RNA expression along the Caenorhabditis elegans germline and, using mutants, dissected gene regulatory mechanisms that control spatio-temporal expression. We detected, at near single-cell resolution, > 10,000 mRNAs, > 300 miRNAs and numerous novel miRNAs. Most RNAs were organized in distinct spatial patterns. Germline-specific miRNAs and their targets were co-localized. Moreover, we observed differential 3’ UTR isoform usage for hundreds of mRNAs. In tumorous gld-2 gld-1 mutants, gene expression was strongly perturbed. In particular, differential 3’ UTR usage was significantly impaired. We propose that PIE-1, a transcriptional repressor, functions to maintain spatial gene expression. Our data also suggest that cpsf-4 and fipp-1 control differential 3’ UTR usage for hundreds of genes. Finally, we constructed a “virtual gonad” enabling “virtual in situ hybridizations” and access to all data (https://shiny.mdc-berlin.de/spacegerm/).


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