scholarly journals Apoptosis of porcine Sertoli cells is inhibited by QKI-5 via regulating CASP8

2019 ◽  
Vol 64 (No. 5) ◽  
pp. 207-215
Author(s):  
Mengdi Liang ◽  
Xin Liu ◽  
Jia Guo ◽  
Yuwei Yang ◽  
Yonghong Zhang ◽  
...  
Keyword(s):  
Sertoli Cells ◽  
Caspase 3 ◽  
Rna Binding ◽  
Rna Binding Protein ◽  
Preliminary Evidence ◽  
Testicular Development ◽  
Caspase 8 ◽  
Proliferation And Apoptosis ◽  
Kh Domain ◽  
The Stability

QKI, a KH domain containing RNA binding, is an RNA-binding protein that is involved in cell proliferation and apoptosis through binding to the QKI response element (QRE) site of its target mRNA. And Caspase 8 (CASP8) and Caspase 3 (CASP3) play important roles in the pathway of apoptosis. The purpose of this study was to investigate the effect of QKI-5 on the apoptosis of Sertoli cells. The experimental results show that pig tissues contain QKI-5, QKI-6 and QKI-7. Overexpression of QKI-5 significantly decreased the mRNA expression of CASP8 (P < 0.05) and the protein expression of CASP8 (P < 0.05). On the contrary, inhibiting QKI-5 increased the expression of CASP8 significantly. Overexpression of QKI-5 significantly reduced the apoptosis of Sertoli cells and promoted cell growth (P < 0.05). Furthermore, QKI-5 specifically reduced the stability of CASP8 mRNA by binding QRE sites on CASP8. Our experiments provide preliminary evidence that QKI-5 induces Sertoli cells proliferation by inhibiting apoptosis, and this may be one of the factors promoting testicular development.

scholarly journals MAC5, an RNA-binding protein, protects pri-miRNAs from SERRATE-dependent exoribonuclease activities

2020 ◽  
Vol 117 (38) ◽  
pp. 23982-23990 ◽  
Author(s):  
Shengjun Li ◽  
Mu Li ◽  
Kan Liu ◽  
Huimin Zhang ◽  
Shuxin Zhang ◽  
...  
Keyword(s):  
Rna Binding ◽  
Rna Binding Protein ◽  
Dual Role ◽  
Mirna Biogenesis ◽  
Core Component ◽  
Stem Loop ◽  
Loop Region ◽  
Nuclear Rna ◽  
Efficient Processing ◽  
The Stability

MAC5 is a component of the conserved MOS4-associated complex. It plays critical roles in development and immunity. Here we report that MAC5 is required for microRNA (miRNA) biogenesis. MAC5 interacts with Serrate (SE), which is a core component of the microprocessor that processes primary miRNA transcripts (pri-miRNAs) into miRNAs and binds the stem-loop region of pri-miRNAs. MAC5 is essential for both the efficient processing and the stability of pri-miRNAs. Interestingly, the reduction of pri-miRNA levels inmac5is partially caused by XRN2/XRN3, the nuclear-localized 5′-to-3′ exoribonucleases, and depends on SE. These results reveal that MAC5 plays a dual role in promoting pri-miRNA processing and stability through its interaction with SE and/or pri-miRNAs. This study also uncovers that pri-miRNAs need to be protected from nuclear RNA decay machinery, which is connected to the microprocessor.

scholarly journals The Putative RNA-Binding Protein Nrp1 Promotes the Loading of Kinesin-14/Klp2 to the Mitotic Spindle and Is Sequestered Into Heat-Induced Protein Aggregates in Fission Yeast

2021 ◽  
Author(s):  
Masashi Yukawa ◽  
Mitsuki Ohishi ◽  
Yusuke Yamada ◽  
Takashi Toda
Keyword(s):  
Fission Yeast ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Protein Aggregates ◽  
Associated Proteins ◽  
Spindle Microtubules ◽  
The Stability ◽  
And Function ◽  
Post Transcriptional Regulation

Cells form a bipolar spindle during mitosis to ensure accurate chromosome segregation. Proper spindle architecture is established by a set of kinesin motors and microtubule-associated proteins. In most eukaryotes, kinesin-5 motors are essential for this process, and genetic or chemical inhibition of their activity leads to the emergence of monopolar spindles and cell death. However, these deficiencies can be rescued by simultaneous inactivation of kinesin-14 motors, as they counteract kinesin-5. We conducted detailed genetic analyses in fission yeast to understand the mechanisms driving spindle assembly in the absence of kinesin-5. Here we show that deletion of the nrp1 gene, which encodes a putative RNA-binding protein with unknown function, can rescue temperature sensitivity caused by cut7-22, a fission yeast kinesin-5 mutant. Interestingly, kinesin-14/Klp2 levels on the spindles in the cut7 mutants were significantly reduced by the nrp1 deletion, although the total levels of Klp2 and the stability of spindle microtubules remained unaffected. Moreover, RNA-binding motifs of Nrp1 are essential for its cytoplasmic localization and function. We have also found that a portion of Nrp1 is spatially and functionally sequestered by chaperone-based protein aggregates upon mild heat stress and limits cell division at high temperatures. We propose that Nrp1 might be involved in post-transcriptional regulation through its RNA-binding ability to promote the loading of Klp2 on the spindle microtubules.

scholarly journals RNA Binding Protein Musashi1 Is Expressed in Sertoli Cells in the Rat Testis from Fetal Life to Adulthood

2002 ◽  
Vol 66 (2) ◽  
pp. 500-507 ◽  
Author(s):  
P.T.K. Saunders ◽  
S.M. Maguire ◽  
S. Macpherson ◽  
M.C. Fenelon ◽  
S. Sakakibara ◽  
...  
Keyword(s):  
Sertoli Cells ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Fetal Life ◽  
Rat Testis

scholarly journals Premature Translation of oskar in Oocytes Lacking the RNA-Binding Protein Bicaudal-C

1998 ◽  
Vol 18 (8) ◽  
pp. 4855-4862 ◽  
Author(s):  
Emma E. Saffman ◽  
Sylvia Styhler ◽  
Katherine Rother ◽  
Weihua Li ◽  
Stéphane Richard ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Point Mutation ◽  
Mammalian Cells ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Rna Binding Protein ◽  
C Protein ◽  
Kh Domain ◽  
Anterior Posterior

ABSTRACT Bicaudal-C (Bic-C) is required duringDrosophila melanogaster oogenesis for several processes, including anterior-posterior patterning. The gene encodes a protein with five copies of the KH domain, a motif found in a number of RNA-binding proteins. Using antibodies raised against the BIC-C protein, we show that multiple isoforms of the protein exist in ovaries and that the protein, like the RNA, accumulates in the developing oocyte early in oogenesis. BIC-C protein expressed in mammalian cells can bind RNA in vitro, and a point mutation in one of the KH domains that causes a strong Bic-C phenotype weakens this binding. In addition, oskar translation commences prior to posterior localization of oskar RNA inBic-C − oocytes, indicating thatBic-C may regulate oskar translation during oogenesis.

scholarly journals The Arabidopsis KH-Domain RNA-Binding Protein ESR1 Functions in Components of Jasmonate Signalling, Unlinking Growth Restraint and Resistance to Stress

PLoS ONE ◽  
2015 ◽  
Vol 10 (5) ◽  
pp. e0126978 ◽  
Author(s):  
Louise F. Thatcher ◽  
Lars G. Kamphuis ◽  
James K. Hane ◽  
Luis Oñate-Sánchez ◽  
Karam B. Singh
Keyword(s):  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Kh Domain ◽  
Resistance To Stress ◽  
Jasmonate Signalling

scholarly journals The RNA-binding protein, Rasputin/G3BP, enhances the stability and translation of its target mRNAs

2020 ◽  
Author(s):  
John D. Laver ◽  
Jimmy Ly ◽  
Allison K. Winn ◽  
Angelo Karaiskakis ◽  
Sichun Lin ◽  
...  
Keyword(s):  
Microarray Analysis ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Rna Binding Protein ◽  
Stress Granules ◽  
Direct Role ◽  
Target Mrnas ◽  
Core Components ◽  
The Stability

SUMMARYG3BP RNA-binding proteins are important components of stress granules (SGs). Here we analyze the role of Drosophila G3BP, Rasputin (RIN), in unstressed cells, where RIN is not SG associated. Immunoprecipitation followed by microarray analysis identified over 550 mRNAs that copurify with RIN. The mRNAs found in SGs are long and translationally silent. In contrast, we find that RIN-bound mRNAs, which encode core components of the transcription, splicing and translation machinery, are short, stable and highly translated. We show that RIN is associated with polysomes and provide evidence for a direct role for RIN and its human homologs in stabilizing and upregulating the translation of their target mRNAs. We propose that when cells are stressed the resulting incorporation of RIN/G3BPs into SGs sequesters them away from their short target mRNAs. This would downregulate the expression of these transcripts, even though they are not incorporated into stress granules.

Proliferation and apoptosis processes in the seasonal testicular development of the wild Daurian ground squirrel (Citellus dauricus Brandt, 1844)

2017 ◽  
Vol 29 (9) ◽  
pp. 1680 ◽  
Author(s):  
Yingying Han ◽  
Jinqi Zhan ◽  
Ying Xu ◽  
Fengwei Zhang ◽  
Zhengrong Yuan ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Breeding Season ◽  
Caspase 3 ◽  
Nuclear Translocation ◽  
Ground Squirrels ◽  
Nuclear Antigen ◽  
Plasma Testosterone ◽  
Testicular Development ◽  
Cyclin D2 ◽  
Proliferation And Apoptosis

The aim of the present study was to elucidate the regulatory role of cell proliferation and apoptosis in testicular development of wild Daurian ground squirrels during the breeding season (April), the non-breeding season (June) and before hibernation (September). Gross mass and hormonal analysis showed that the testis : body mass ratio and plasma testosterone concentration fluctuated seasonally, with a peak in April and lowest values in June. Similarly, spermatogenesis was fully developed in April but suppressed in June and September. Testicular decellularisation and vacuolisation was seen during the transition from the breeding to the non-breeding season. Furthermore, testicular levels of proliferating cell nuclear antigen, cyclin D2 and caspase-3 protein were significantly increased in June and September. Intriguingly, positive terminal deoxyribonucleotidyl transferase-mediated dUTP–digoxigenin nick end-labelling staining and nuclear translocation of caspase-3 in testicular germ cells appeared only during the prehibernation period, whereas accumulation of cyclin D2 in spermatocyte nuclei occurred in September. These findings demonstrate, for the first time, that both cell proliferation and apoptosis are stimulated during the prehibernation period, indicating that a hormonal-regulated balance of testicular germ cell proliferation and apoptosis may play a pivotal role in preparing for testicular recrudescence of wild Daurian ground squirrels.

scholarly journals MicroRNA-155 Promotes Myocardial Infarction-Induced Apoptosis by Targeting RNA-Binding Protein QKI

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Jing Guo ◽  
Hui-Bin Liu ◽  
Chuan Sun ◽  
Xiu-Qing Yan ◽  
Juan Hu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Rna Binding ◽  
Apoptotic Cell ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Cell Number ◽  
Neonatal Rat

Acute myocardial infarction (AMI) is the leading cause of sudden death worldwide. MicroRNA-155 (miR-155) has been reported to target antiapoptotic genes in various diseases models, but the functional role of miR-155 in response to MI injury needs further investigations. This study investigated the role of miR-155 in myocardial ischemia injury. TUNEL and flow cytometry were performed to measure cell apoptosis. Western blot analysis was employed to detect protein expressions of Bcl-2, XIAP, Bax, and caspase-3. qRT-PCR was used to quantify miRNA levels. We showed that miR-155 was dynamically elevated in murine hearts subjected to MI and in neonatal rat ventricular cardiomyocyte (NRVM) injury induced by hydrogen peroxide (H2O2). In response to H2O2, the silencing of miR-155 using AMO-155 (antisense inhibitor oligodeoxyribonucleotides) significantly increased cell viability and reduced cell apoptosis. Moreover, AMO-155 reversed the H2O2-induced downregulation of Bcl-2 and XIAP and upregulation of Bax and cleaved-caspase-3. Further study revealed that AMO-155 resulted in a decrease of H2O2-induced JC-1-labelled monomeric cell number. In addition, AMO-155 markedly decreased infarct size, ameliorated impaired cardiac function, and significantly reduced apoptotic cell percentages in MI mice heart. The RNA-binding protein Quaking (QKI) was predicted as a target gene of miR-155 through bioinformatic analysis, and AMO-155 attenuated the downregulation of QKI in H2O2-treated cardiomyocytes and MI mice heart. Knockdown of QKI by siRNA abolished the antiapoptotic effects of AMO-155. Taken together, miR-155 is upregulated in the MI heart and NRVMs in response to H2O2 stress, and downregulating of miR-155 protects cardiomyocytes against apoptosis. Mechanistically, it is probably due to the repression of QKI signaling pathway.

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