Genetic compensation: A phenomenon in search of mechanisms.
TLDR
This review revisits studies reporting genetic compensation in higher eukaryotes and outlines possible molecular mechanisms, which may include both transcriptional and posttranscriptional processes.Abstract:
Several recent studies in a number of model systems including zebrafish, Arabidopsis, and mouse have revealed phenotypic differences between knockouts (i.e., mutants) and knockdowns (e.g., antisense-treated animals). These differences have been attributed to a number of reasons including off-target effects of the antisense reagents. An alternative explanation was recently proposed based on a zebrafish study reporting that genetic compensation was observed in egfl7 mutant but not knockdown animals. Dosage compensation was first reported in Drosophila in 1932, and genetic compensation in response to a gene knockout was first reported in yeast in 1969. Since then, genetic compensation has been documented many times in a number of model organisms; however, our understanding of the underlying molecular mechanisms remains limited. In this review, we revisit studies reporting genetic compensation in higher eukaryotes and outline possible molecular mechanisms, which may include both transcriptional and posttranscriptional processes.read more
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Slc2a10 knock-out mice deficient in ascorbic acid synthesis recapitulate aspects of arterial tortuosity syndrome and display mitochondrial respiration defects
Annekatrien Boel,Annekatrien Boel,Joyce Burger,Marine Vanhomwegen,Aude Beyens,Aude Beyens,Marjolijn Renard,Sander Barnhoorn,Christophe Casteleyn,Dieter P. Reinhardt,Benedicte Descamps,Christian Vanhove,Ingrid van der Pluijm,Paul Coucke,Andy Willaert,Jeroen Essers,Bert Callewaert +16 more
TL;DR: Evidence is added that ATS is an ascorbate compartmentalization disorder, but additional factors underlying the observed phenotype in humans remain to be determined.
Journal ArticleDOI
Lack of the myotendinous junction marker col22a1 results in posture and locomotion disabilities in zebrafish.
Marilyne Malbouyres,Alexandre Guiraud,Christel Lefrançois,Mélanie Salamito,Pauline Nauroy,Laure Bernard,Frédéric Sohm,Bruno Allard,Florence Ruggiero +8 more
TL;DR: The myotendinous junction (MTJ) is essential for the integrity of the musculoskeletal unit, and gene ablation of the MTJ marker col22a1 in zebrafish results in MTJ dysfunction but with variable degrees of expression and distinct phenotypic classes as discussed by the authors .
Journal ArticleDOI
RNAi as a Tool to Study Virulence in the Pathogenic Yeast Candida glabrata
Olena P. Ishchuk,Khadija Mohamed Ahmad,Katarina Koruza,Klara Bojanovič,Marcel Sprenger,Lydia Kasper,Sascha Brunke,Bernhard Hube,Torbjörn Säll,Thomas Hellmark,Birgitta Gullstrand,Christian Brion,Kelle C. Freel,Joseph Schacherer,Birgitte Regenberg,Wolfgang Knecht,Jure Piškur +16 more
TL;DR: Phenotypic profiling with a high-resolution quantification of growth identified genes involved in the maintenance of cell integrity, antifungal drugs, and ROS resistance that are promising targets for the treatment of C. glabrata infections.
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Mitochondrial TSPO Deficiency Triggers Retrograde Signaling in MA-10 Mouse Tumor Leydig Cells.
Jinjiang Fan,Jinjiang Fan,Vassilios Papadopoulos,Vassilios Papadopoulos,Vassilios Papadopoulos +4 more
TL;DR: In this article, the authors explored the consequences of TSPO depletion via CRISPR-Cas9-mediated deletion (indel) mutation in MA-10 cells using RNA-seq.
Journal ArticleDOI
Corticosteroid treatment exacerbates nephrotic syndrome in a zebrafish model of magi2a knockout.
Tilman Jobst-Schwan,Charlotte A. Hoogstraten,Caroline M. Kolvenbach,Johanna Magdalena Schmidt,Amy Kolb,Kaitlyn Eddy,Ronen Schneider,Shazia Ashraf,Eugen Widmeier,Amar J. Majmundar,Friedhelm Hildebrandt +10 more
TL;DR: In the first CRISPR/Cas9 zebrafish knockout model of SRNS, it is found that corticosteroids may have a paradoxical effect in the setting of specific genetic mutations.
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