RNAi (RNA-mediated genetic interference)

2012 ◽  
Keyword(s):  
Genetic Interference

scholarly journals Models for Chromatid Interference With Applications to Recombination Data

Genetics ◽  
2000 ◽  
Vol 156 (3) ◽  
pp. 1449-1460
Author(s):  
F Teuscher ◽  
G A Brockmann ◽  
P E Rudolph ◽  
H H Swalve ◽  
V Guiard
Keyword(s):  
Real Data ◽  
New Model ◽  
The Third ◽  
Genetic Interference ◽  
Three Components

Abstract Genetic interference means that the occurrence of one crossover affects the occurrence and/or location of other crossovers in its neighborhood. Of the three components of genetic interference, two are well modeled: the distribution of the number and the locations of chiasmata. For the third component, chromatid interference, there exists only one model. Its application to real data has not yet been published. A further, new model for chromatid interference is presented here. In contrast to the existing model, it is assumed that chromatid interference acts only in the neighborhood of a chiasma. The appropriateness of this model is demonstrated by its application to three sets of recombination data. Both models for chromatid interference increased fit significantly compared to assuming no chromatid interference, at least for parts of the chromosomes. Interference does not necessarily act homogeneously. After extending both models to allow for heterogeneity of chromatid interference, a further improvement in fit was achieved.

scholarly journals Stem cells and fluid flow drive cyst formation in an invertebrate excretory organ

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Hanh Thi-Kim Vu ◽  
Jochen C Rink ◽  
Sean A McKinney ◽  
Melainia McClain ◽  
Naharajan Lakshmanaperumal ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Kidney Diseases ◽  
Human Kidney ◽  
Cyst Formation ◽  
Cystic Kidney ◽  
Flow Sensing ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Genetic Interference ◽  
Cystic Kidney Diseases

Cystic kidney diseases (CKDs) affect millions of people worldwide. The defining pathological features are fluid-filled cysts developing from nephric tubules due to defective flow sensing, cell proliferation and differentiation. The underlying molecular mechanisms, however, remain poorly understood, and the derived excretory systems of established invertebrate models (Caenorhabditis elegans and Drosophila melanogaster) are unsuitable to model CKDs. Systematic structure/function comparisons revealed that the combination of ultrafiltration and flow-associated filtrate modification that is central to CKD etiology is remarkably conserved between the planarian excretory system and the vertebrate nephron. Consistently, both RNA-mediated genetic interference (RNAi) of planarian orthologues of human CKD genes and inhibition of tubule flow led to tubular cystogenesis that share many features with vertebrate CKDs, suggesting deep mechanistic conservation. Our results demonstrate a common evolutionary origin of animal excretory systems and establish planarians as a novel and experimentally accessible invertebrate model for the study of human kidney pathologies.

Potent and specific genetic interference by double-stranded RNA in Caenorhabditis elegans

Nature ◽  
10.1038/35888 ◽  
1998 ◽  
Vol 391 (6669) ◽  
pp. 806-811 ◽  
Author(s):  
Andrew Fire ◽  
SiQun Xu ◽  
Mary K. Montgomery ◽  
Steven A. Kostas ◽  
Samuel E. Driver ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Double Stranded Rna ◽  
Genetic Interference

scholarly journals Xyloglucan Remodeling Defines Auxin-Dependent Differential Tissue Expansion in Plants

2021 ◽  
Vol 22 (17) ◽  
pp. 9222 ◽  
Author(s):  
Silvia Melina Velasquez ◽  
Xiaoyuan Guo ◽  
Marçal Gallemi ◽  
Bibek Aryal ◽  
Peter Venhuizen ◽  
...  
Keyword(s):  
Cell Wall ◽  
Growth Control ◽  
Size Control ◽  
Tissue Expansion ◽  
Major Type ◽  
Hypocotyl Growth ◽  
Differential Growth ◽  
Rigid Cell Wall ◽  
Molecular Complexity ◽  
Genetic Interference

Size control is a fundamental question in biology, showing incremental complexity in plants, whose cells possess a rigid cell wall. The phytohormone auxin is a vital growth regulator with central importance for differential growth control. Our results indicate that auxin-reliant growth programs affect the molecular complexity of xyloglucans, the major type of cell wall hemicellulose in eudicots. Auxin-dependent induction and repression of growth coincide with reduced and enhanced molecular complexity of xyloglucans, respectively. In agreement with a proposed function in growth control, genetic interference with xyloglucan side decorations distinctly modulates auxin-dependent differential growth rates. Our work proposes that auxin-dependent growth programs have a spatially defined effect on xyloglucan’s molecular structure, which in turn affects cell wall mechanics and specifies differential, gravitropic hypocotyl growth.

scholarly journals Context-dependent requirement of H3K9 methyltransferase activity during cellular reprogramming to iPSCs

2019 ◽  
Author(s):  
Simon Vidal ◽  
Alexander Polyzos ◽  
Jorge Morales Valencia ◽  
Hongsu Wang ◽  
Emily Swanzey ◽  
...  
Keyword(s):  
Pluripotent Stem Cells ◽  
Cellular Reprogramming ◽  
Methyltransferase Activity ◽  
Molecular Defects ◽  
Functional Interactions ◽  
Histone 3 ◽  
Epigenetic Remodeling ◽  
Genetic Interference ◽  
Induced Pluripotent ◽  
Epithelial State

SUMMARYMethylation of histone 3 at lysine 9 (H3K9) is widely regarded as a major roadblock for cellular reprogramming and interference with associated methyltransferases such as EHMT1 and EHMT2 (also known as GLP and G9A, respectively) increases the efficiencies at which induced pluripotent stem cells (iPSCs) can be derived. Activation of histone and DNA demethylases by ascorbic acid (AA) has become a common approach to facilitate the extensive epigenetic remodeling required for iPSC formation, but possible functional interactions between the H3K9 methylation machinery and AA-stimulated enzymes remain insufficiently explored. Here we show that reduction of EHMT1/2 activity counteracts iPSC formation in an optimized reprogramming system in the presence of AA. Mechanistically, EHMT1/2 activity under these conditions is required for efficient downregulation of somatic genes and transition into an epithelial state. Of note, transient inhibition of EHMT1/2 during reprogramming yields iPSCs that fail to efficiently give rise to viable mice, suggesting persistent molecular defects in these cells. Genetic interference with the H3K9 demethylase KDM3B ameliorated the adverse effect of EHMT1/2 inhibition on iPSC formation. Together, our observations document novel functions of H3K9 methyltransferases during iPSC formation and suggest that the balancing of AA-stimulated enzymes by EHMT1/2 supports efficient and error-free iPSC reprogramming to pluripotency.

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