Conditional inhibition of β-glucuronidase expression by antisense gene fragments in petunia protoplasts

1993 ◽  
Vol 23 (1) ◽  
pp. 45-55 ◽  
Author(s):  
Pieter de Lange ◽  
Gert-Jan de Boer ◽  
Joseph N. M. Mol ◽  
Jan M. Kooter

Genetics ◽  
2001 ◽  
Vol 157 (4) ◽  
pp. 1723-1733
Author(s):  
Francesca Ros ◽  
Reinhard Kunze

Abstract In maize the transposable elements Activator/Dissociation (Ac/Ds) transpose shortly after replication from one of the two resulting chromatids (“chromatid selectivity”). A model has been suggested that explains this phenomenon as a consequence of different affinity for Ac transposase binding to holo-, hemi-, and unmethylated transposon ends. Here we demonstrate that in petunia cells a holomethylated Ds is unable to excise from a nonreplicating vector and that replication restores excision. A Ds element hemi-methylated on one DNA strand transposes in the absence of replication, whereas hemi-methylation of the complementary strand causes a >6.3-fold inhibition of Ds excision. Consistently in the active hemi-methylated state, the Ds ends have a high binding affinity for the transposase, whereas binding to inactive ends is strongly reduced. These results provide strong evidence for the above-mentioned model. Moreover, in the absence of DNA methylation, replication enhances Ds transposition in petunia protoplasts >8-fold and promotes formation of a predominant excision footprint. Accordingly, replication also has a methylation-independent regulatory effect on transposition.



2010 ◽  
Vol 53 (1) ◽  
pp. 313-318 ◽  
Author(s):  
L. J. Xie ◽  
Y. B. Ying ◽  
M. L. Chen ◽  
T. J. Ying


1991 ◽  
Vol 3 (2) ◽  
pp. 22-26
Author(s):  
Xu Xiulan ◽  
Jia Libin ◽  
Zheng Yahai ◽  
Gan Chen ◽  
Gu Jianren ◽  
...  


2003 ◽  
Author(s):  
Hiroshi Yamashita ◽  
Kaneyuki Kubushiro ◽  
Jun Ma ◽  
Takuma Fujii ◽  
Katsumi Tsukazaki ◽  
...  


Gene Therapy ◽  
2000 ◽  
Vol 7 (22) ◽  
pp. 1906-1914 ◽  
Author(s):  
S Endo ◽  
Q Zeng ◽  
N A Burke ◽  
Y He ◽  
M F Melhem ◽  
...  


Author(s):  
O. N. Reznik ◽  
A. E. Skvortsov ◽  
D. O. Kuzmin ◽  
A. P. Tutin ◽  
A. O. Reznik




2019 ◽  
Author(s):  
Xuelian Ma ◽  
Xiaomin Zhao ◽  
Kaili Wang ◽  
Xiaoyi Tang ◽  
Jianxiong Guo ◽  
...  

Abstract Abstract Background: Transmissible gastroenteritis virus (TGEV) infection can cause acute inflammation. Long noncoding RNAs (lncRNAs) play important roles in a number of biological process including inflammation response. However, whether lncRNAs participate in TGEV-induced inflammation in porcine intestinal epithelial cells (IPECs) is largely unknown. Results: In this study, the next-generation sequencing (NGS) technology was used to analyze the profiles of lncRNAs in Mock and TGEV-infected porcine intestinal epithelial cell-jejunum 2 (IPEC-J2) cell line. A total of 106 lncRNAs were differentially expressed. Many differentially expressed lncRNAs act as elements to competitively attach microRNAs (miRNAs) which target to messenger RNA (mRNAs ) to mediate expression of genes that related to Toll-like receptors (TLRs), NOD-like receptors (NLRs), Tumor necrosis factor (TNF), and RIG-I-like receptor s (RLRs) pathways. Functional analysis of the binding proteins and the up/down-stream genes of the differentially expressed lncRNAs revealed that lncRNAs were principally related to inflammatory response. Meanwhile, we found that the differentially expressed lncRNA TCONS_00058367 might lead to a reduction of phosphorylation of transcription factor p65 (p-p65) in TGEV-infected IPEC-J2 cells by negatively regulating its antisense gene romyelocytic leukemia (PML ). Conclusions: The data showed that differentially expressed lncRNAs might be involved in inflammatory response induced by TGEV through acting as miRNA sponges, regulating their up/down-stream genes, or directly binding proteins.



2021 ◽  
Vol 118 (17) ◽  
pp. e2014783118
Author(s):  
Guangyong Ma ◽  
Jun-ichirou Yasunaga ◽  
Kazuya Shimura ◽  
Keiko Takemoto ◽  
Miho Watanabe ◽  
...  

Human retroviruses, including human T cell leukemia virus type 1 (HTLV-1) and HIV type 1 (HIV-1), encode an antisense gene in the negative strand of the provirus. Besides coding for proteins, the messenger RNAs (mRNAs) of retroviral antisense genes have also been found to regulate transcription directly. Thus, it has been proposed that retroviruses likely localize their antisense mRNAs to the nucleus in order to regulate nuclear events; however, this opposes the coding function of retroviral antisense mRNAs that requires a cytoplasmic localization for protein translation. Here, we provide direct evidence that retroviral antisense mRNAs are localized predominantly in the nuclei of infected cells. The retroviral 3′ LTR induces inefficient polyadenylation and nuclear retention of antisense mRNA. We further reveal that retroviral antisense RNAs retained in the nucleus associate with chromatin and have transcriptional regulatory function. While HTLV-1 antisense mRNA is recruited to the promoter of C-C chemokine receptor type 4 (CCR4) and enhances transcription from it to support the proliferation of HTLV-1–infected cells, HIV-1 antisense mRNA is recruited to the viral LTR and inhibits sense mRNA expression to maintain the latency of HIV-1 infection. In summary, retroviral antisense mRNAs are retained in nucleus, act like long noncoding RNAs instead of mRNAs, and contribute to viral persistence.



2016 ◽  
Vol 138 (29) ◽  
pp. 9097-9100 ◽  
Author(s):  
Xueguang Lu ◽  
Fei Jia ◽  
Xuyu Tan ◽  
Dali Wang ◽  
Xueyan Cao ◽  
...  


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