scholarly journals Down-regulation of Fusarium oxysporum endogenous genes by Host-Delivered RNA interference enhances disease resistance

2015 ◽  
Vol 3 ◽  
Author(s):  
Zongli Hu ◽  
Urvi Parekh ◽  
Natsumi Maruta ◽  
Yuri Trusov ◽  
Jose R. Botella
Keyword(s):  
Disease Resistance ◽  
Rna Interference ◽  
Fusarium Oxysporum ◽  
Down Regulation ◽  
Endogenous Genes

scholarly journals Mice with ribosomal protein S19 deficiency develop bone marrow failure and symptoms like patients with Diamond-Blackfan anemia

Blood ◽  
2011 ◽  
Vol 118 (23) ◽  
pp. 6087-6096 ◽  
Author(s):  
Pekka Jaako ◽  
Johan Flygare ◽  
Karin Olsson ◽  
Ronan Quere ◽  
Mats Ehinger ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Rna Interference ◽  
Ribosomal Protein ◽  
Mouse Models ◽  
Bone Marrow Failure ◽  
Macrocytic Anemia ◽  
Down Regulation ◽  
Hematopoietic Stem ◽  
Diamond Blackfan Anemia ◽  
Ribosomal Protein S19

Abstract Diamond-Blackfan anemia (DBA) is a congenital erythroid hypoplasia caused by a functional haploinsufficiency of genes encoding for ribosomal proteins. Among these genes, ribosomal protein S19 (RPS19) is mutated most frequently. Generation of animal models for diseases like DBA is challenging because the phenotype is highly dependent on the level of RPS19 down-regulation. We report the generation of mouse models for RPS19-deficient DBA using transgenic RNA interference that allows an inducible and graded down-regulation of Rps19. Rps19-deficient mice develop a macrocytic anemia together with leukocytopenia and variable platelet count that with time leads to the exhaustion of hematopoietic stem cells and bone marrow failure. Both RPS19 gene transfer and the loss of p53 rescue the DBA phenotype implying the potential of the models for testing novel therapies. This study demonstrates the feasibility of transgenic RNA interference to generate mouse models for human diseases caused by haploinsufficient expression of a gene.

RNA Interference Mechanisms and Applications in Plant Pathology

2018 ◽  
Vol 56 (1) ◽  
pp. 581-610 ◽  
Author(s):  
Cristina Rosa ◽  
Yen-Wen Kuo ◽  
Hada Wuriyanghan ◽  
Bryce W. Falk
Keyword(s):  
Plant Pathology ◽  
Rna Interference ◽  
Gene Function ◽  
Small Rnas ◽  
Plant Pathogens ◽  
Common Ancestor ◽  
Plant Protection ◽  
Plant Diseases ◽  
Antiviral Defense ◽  
Endogenous Genes

The origin of RNA interference (RNAi), the cell sentinel system widely shared among eukaryotes that recognizes RNAs and specifically degrades or prevents their translation in cells, is suggested to predate the last eukaryote common ancestor ( 138 ). Of particular relevance to plant pathology is that in plants, but also in some fungi, insects, and lower eukaryotes, RNAi is a primary and effective antiviral defense, and recent studies have revealed that small RNAs (sRNAs) involved in RNAi play important roles in other plant diseases, including those caused by cellular plant pathogens. Because of this, and because RNAi can be manipulated to interfere with the expression of endogenous genes in an intra- or interspecific manner, RNAi has been used as a tool in studies of gene function but also for plant protection. Here, we review the discovery of RNAi, canonical mechanisms, experimental and translational applications, and new RNA-based technologies of importance to plant pathology.

scholarly journals Essential Notes Regarding the Design of Functional siRNAs for Efficient Mammalian RNAi

2006 ◽  
Vol 2006 ◽  
pp. 1-8 ◽  
Author(s):  
Kumiko Ui-Tei ◽  
Yuki Naito ◽  
Kaoru Saigo
Keyword(s):  
Rna Interference ◽  
Mammalian Cells ◽  
Target Gene ◽  
Software Systems ◽  
Sirna Sequence ◽  
Web Based ◽  
Sequence Selection ◽  
Endogenous Genes ◽  
Selection Algorithms ◽  
Online Software

Short interfering RNAs (siRNAs) are widely used to bring about RNA interference (RNAi) in mammalian cells. Numerous siRNAs may be designed for any target gene though most of which would be incapable of efficiently inducing mammalian RNAi. Certain highly functional siRNAs designed for knockout of a particular gene may render unrelated endogenous genes nonfunctional. These major bottlenecks should be properly eliminated when RNAi technologies are employed for any experiment in mammalian functional genomics. This paper thus presents essential notes and findings regarding the proper choice of siRNA-sequence selection algorithms and web-based online software systems.

scholarly journals HOXD8/DIAPH2-AS1 epigenetically regulates PAX3 and impairs HTR-8/SVneo cell function under hypoxia

2019 ◽  
Vol 39 (1) ◽  
Author(s):  
Yaling Feng ◽  
Jianxia Wang ◽  
Yue He ◽  
Heng Zhang ◽  
Minhui Jiang ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Rna Interference ◽  
Chromatin Immunoprecipitation ◽  
Regulatory Network ◽  
Molecular Basis ◽  
Promoter Region ◽  
Cell Function ◽  
Down Regulation ◽  
Histone 3 ◽  
Development Data

Abstract The present study aimed to unravel the molecular basis underlying PAX3 down-regulation, known to be involved in pre-eclampsia (PE) occurrence and development. Data obtained from databases suggested that Pax3 methylation levels in the promoter region are high in the placentas of PE patients. However, the expression of methylation-adjusting enzymes, including DNMT1, LSD1, and EZH2, did not change. Since lncRNAs enhance the function of methylation-related enzymes independently of expression, we selected three lncRNAs, RP11-269F21.2, DIAPH2-AS1, and RP11-445K13.2, predicted to interact with methylation-adjusting enzymes. Two transcription factors, HOXD8 and Lhx3, predicted to regulate the expression of lncRNAs, were also selected. Using RNA interference technology, HOXD8 and Lhx3 were found to positively regulate DIAPH2-AS1 and RP11-445K13.2 in HTR-8/SVneo cells. Chromatin immunoprecipitation assays determined that DIAPH2-AS1 recruited LSD1 to histone 3, increasing DNMT1 stability at H3. The HOXD8/DIAPH2-AS1 network regulated HTR-8/SVneo cell function under hypoxia by epigenetically regulating PAX3. This regulatory network may thus be responsible for PAX3 down-regulation in the placentas of PE patients.

scholarly journals Involvement of Human MCM8 in Prereplication Complex Assembly by Recruiting hcdc6 to Chromatin

2005 ◽  
Vol 25 (4) ◽  
pp. 1560-1568 ◽  
Author(s):  
Melanie Volkening ◽  
Ingrid Hoffmann
Keyword(s):  
Rna Interference ◽  
Dna Replication ◽  
S Phase ◽  
Protein Family ◽  
Down Regulation ◽  
Complex Assembly ◽  
Essential Component ◽  
Crucial Component

ABSTRACT The MCM2-MCM7 complex is an essential component of the prereplication complex (pre-RC), which is recruited by the cdc6 and cdt1 proteins to origins of DNA replication during G1 phase. Here, we report that the accumulation on chromatin of another member of the MCM protein family, human MCM8 (hMCM8), occurs during early G1 phase, before the hMCM2-hMCM7 complex binds. hMCM8 interacts in vivo with two components of the pre-RC, namely, hcdc6 and hORC2. Depletion of endogenous hMCM8 protein by RNA interference leads to a delay of entry into S phase, suggesting a role for hMCM8 in G1 progression. Furthermore, down-regulation of hMCM8 also leads to a reduced loading of hcdc6 and the hMCM2-hMCM7 complex on chromatin. These results suggest that hMCM8 is a crucial component of the pre-RC and that the interaction between hMCM8 and hcdc6 is required for pre-RC assembly.

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