Characterisation of a T-DNA-tagged gene of Arabidopsis thaliana that regulates gibberellin metabolism and flowering time

2005 ◽  
Vol 32 (10) ◽  
pp. 923 ◽  
Author(s):  
Maria Svensson ◽  
Dan Lundh ◽  
Per Bergman ◽  
Abul Mandal
Keyword(s):  
Arabidopsis Thaliana ◽  
Flowering Time ◽  
Rna Binding ◽  
Binding Protein ◽  
Sequence Similarity ◽  
Rna Binding Protein ◽  
Transcriptional Level ◽  
Root Tips ◽  
Gibberellin Metabolism ◽  
Ga Biosynthesis

A gene (At4g20010) involved in regulating flowering time in Arabidopsis thaliana (L.) Heynh. was identified by promoter trap T-DNA tagging. Plants containing a T-DNA insert in the 3′-UTR of At4g20010 flowered later under both long- and short-day conditions compared with control plants. Histochemical assays of the mutant plants showed that the promoterless gus gene is expressed predominantly in the shoot apex, but it is also expressed in root tips, stem nodes and in the abscission zone of developing siliques. Measurement of endogenous gibberellin (GA) showed that bioactive GA4 levels in mutant plants were reduced compared with wild type (WT) plants. Like other known mutants defective in GA biosynthesis, the late-flowering phenotype observed in our T-DNA-tagged line could be largely repressed by application of exogenous GA3. The T-DNA-tagged gene At4g20010 encodes a previously uncharacterised protein belonging to the DUF731 family. Sequence analysis showed similarity to a single-stranded binding domain and to an RNA-binding protein of Chlamydomonas reinhardtii. Considering the above results (sequence similarity, mutant phenotype and level of endogenous GA), we propose that At4g20010 is an RNA-binding protein involved in regulating GA biosynthesis, possibly at the post-transcriptional level.

The small glycine-rich RNA binding protein At GRP7 promotes floral transition in Arabidopsis thaliana

2008 ◽  
Vol 56 (2) ◽  
pp. 239-250 ◽  
Author(s):  
Corinna Streitner ◽  
Selahattin Danisman ◽  
Franziska Wehrle ◽  
Jan C. Schöning ◽  
James R. Alfano ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Floral Transition

Double-stranded RNA-binding protein DRB3 negatively regulates anthocyanin biosynthesis by modulating PAP1 expression in Arabidopsis thaliana

2016 ◽  
Vol 130 (1) ◽  
pp. 45-55 ◽  
Author(s):  
Hikaru Sawano ◽  
Takuma Matsuzaki ◽  
Tomoyuki Usui ◽  
Midori Tabara ◽  
Akihito Fukudome ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Rna Binding ◽  
Anthocyanin Biosynthesis ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Double Stranded Rna

scholarly journals The RNA‐binding protein RBP45D of Arabidopsis promotes transgene silencing and flowering time

2021 ◽  
Author(s):  
Liangsheng Wang ◽  
Duorong Xu ◽  
Kristin Scharf ◽  
Wolfgang Frank ◽  
Dario Leister ◽  
...  
Keyword(s):  
Flowering Time ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Transgene Silencing

scholarly journals Coordinated post-transcriptional control of oncogene-induced senescence by UNR/CSDE1

2020 ◽  
Author(s):  
Rosario Avolio ◽  
Marta Inglés-Ferrandiz ◽  
Annagiulia Ciocia ◽  
Sarah Bonnin ◽  
Anna Ribó ◽  
...  
Keyword(s):  
Transcriptional Control ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Tumor Formation ◽  
Transcriptional Level ◽  
Melanoma Metastasis ◽  
Primary Mouse ◽  
Mouse Keratinocytes

SUMMARYOncogene-induced senescence (OIS) is a form of stable cell cycle arrest elicited in cells as a response to oncogenic stimulation. OIS must be bypassed for transformation, but the mechanisms of OIS establishment and bypass remain poorly understood, especially at the post-transcriptional level. Here we show that the RNA binding protein UNR/CSDE1, previously involved in melanoma metastasis, unexpectedly enables OIS in primary mouse keratinocytes that have been challenged by over-expression of oncogenic H-Ras. Depletion of CSDE1 leads to senescence bypass, cell immortalization and tumor formation in vivo, indicating that CSDE1 behaves as a tumor suppressor. Using iCLIP-Seq, RNA-Seq and polysome profiling we have uncovered two independent molecular branches by which CSDE1 contributes to OIS. On one hand, CSDE1 enhances the senescence-associated secretory phenotype (SASP) by promoting the stability of SASP factor mRNAs. On the other hand, CSDE1 represses the synthesis of the pro-oncogenic RNA binding protein YBX1. Importantly, depletion of YBX1 from immortal keratinocytes rescues senescence and uncouples proliferation arrest from the SASP, revealing multilayered post-transcriptional mechanisms exerted by CSDE1 to control senescence. Our data uncover a novel function of CSDE1, and highlight the relevance of post-transcriptional control in the regulation of senescence.

scholarly journals Post-transcriptional regulation of MEK-1 by polyamines through the RNA-binding protein HuR modulating intestinal epithelial apoptosis

2010 ◽  
Vol 426 (3) ◽  
pp. 293-306 ◽  
Author(s):  
Peng-Yuan Wang ◽  
Jaladanki N. Rao ◽  
Tongtong Zou ◽  
Lan Liu ◽  
Lan Xiao ◽  
...  
Keyword(s):  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Mitogen Activated Protein Kinase ◽  
Transcriptional Level ◽  
Intestinal Epithelial ◽  
Cellular Functions ◽  
Mitogen Activated Protein ◽  
Hu Antigen R ◽  
Post Transcriptional Regulation

MEK-1 [MAPK (mitogen-activated protein kinase) kinase-1] is an important signal transducing enzyme that is implicated in many aspects of cellular functions. In the present paper, we report that cellular polyamines regulate MEK-1 expression at the post-transcriptional level through the RNA-binding protein HuR (Hu-antigen R) in IECs (intestinal epithelial cells). Decreasing the levels of cellular polyamines by inhibiting ODC (ornithine decarboxylase) stabilized MEK-1 mRNA and promoted its translation through enhancement of the interaction between HuR and the 3′-untranslated region of MEK-1 mRNA, whereas increasing polyamine levels by ectopic ODC overexpression destabilized the MEK-1 transcript and repressed its translation by reducing the abundance of HuR–MEK-1 mRNA complex; neither intervention changed MEK-1 gene transcription via its promoter. HuR silencing rendered the MEK-1 mRNA unstable and inhibited its translation, thus preventing increases in MEK-1 mRNA and protein in polyamine-deficient cells. Conversely, HuR overexpression increased MEK-1 mRNA stability and promoted its translation. Inhibition of MEK-1 expression by MEK-1 silencing or HuR silencing prevented the increased resistance of polyamine-deficient cells to apoptosis. Moreover, HuR overexpression did not protect against apoptosis if MEK-1 expression was silenced. These results indicate that polyamines destabilize the MEK-1 mRNA and repress its translation by inhibiting the association between HuR and the MEK-1 transcript. Our findings indicate that MEK-1 is a key effector of the HuR-elicited anti-apoptotic programme in IECs.

The RNA-binding protein HuR stabilizes survivin mRNA in human oesophageal epithelial cells

2011 ◽  
Vol 437 (1) ◽  
pp. 89-96 ◽  
Author(s):  
James M. Donahue ◽  
Elizabeth T. Chang ◽  
Lan Xiao ◽  
Peng-Yuan Wang ◽  
Jaladanki N. Rao ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Oesophageal Cancer ◽  
Mrna Stability ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Survivin Expression ◽  
Transcriptional Level ◽  
Survivin Mrna ◽  
Hu Antigen R

Overexpression of survivin, a member of the IAP (inhibitor of apoptosis) family, has been correlated with poorer outcomes in multiple malignancies, including oesophageal cancer. The regulatory mechanisms, particularly at the post-transcriptional level, involved in survivin overexpression are not well understood. Previous work from our group has shown that the RNA-binding protein HuR (Hu antigen R), which is also overexpressed in several malignancies, stabilizes the mRNA of XIAP (X-linked IAP), another IAP family member. In the present study, we demonstrate the binding of HuR to a 288 bp fragment in the 3′-UTR (untranslated region) of survivin mRNA in human oesophageal epithelial cells. Unexpectedly, overexpression of HuR led to a decrease in survivin expression. This was associated with decreased survivin mRNA and promoter activity, suggesting a decrease in transcription. Levels of p53, a negative transcriptional regulator of survivin, increased following HuR overexpression, in conjunction with enhanced p53 mRNA stability. Silencing p53 prior to HuR overexpression resulted in increased survivin protein and mRNA stability. These results demonstrate that, in the absence of p53, HuR overexpression results in increased survivin mRNA stability and protein expression. This provides an additional explanation for the increased survivin expression observed in oesophageal cancer cells that have lost p53.

scholarly journals The Role of Cold Inducible RNA-Binding Protein in Cardiac Physiology and Diseases

2021 ◽  
Vol 12 ◽  
Author(s):  
Peng Zhong ◽  
Jianye Peng ◽  
Zhouyan Bian ◽  
He Huang
Keyword(s):  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Stress Conditions ◽  
Telomere Maintenance ◽  
Transcriptional Level ◽  
Cardiac Physiology ◽  
Electrophysiological Properties ◽  
Kidney Liver

Cold-inducible RNA-binding protein (CIRP) is an intracellular stress-response protein that can respond to various stress conditions by changing its expression and regulating mRNA stability. As an RNA-binding protein, CIRP modulates gene expression at the post-transcriptional level, including those genes involved in DNA repair, cellular redox metabolism, circadian rhythms, telomere maintenance, and cell survival. CIRP is expressed in a large variety of tissues, including testis, brain, lung, kidney, liver, stomach, bone marrow, and heart. Recent studies have observed the important role of CIRP in cardiac physiology and diseases. CIRP regulates cardiac electrophysiological properties such as the repolarization of cardiomyocytes, the susceptibility of atrial fibrillation, and the function of the sinoatrial node in response to stress. CIRP has also been suggested to protect cardiomyocytes from apoptosis under various stress conditions, including heart failure, high glucose conditions, as well as during extended heart preservation under hypothermic conditions. This review summarizes the findings of CIRP investigations in cardiac physiology and diseases and the underlying molecular mechanism.

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