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Open AccessJournal ArticleDOI

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.

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Journal Article

Genetic compensation induced by deleterious mutations but not gene knockdowns

TL;DR: In this article, the authors show that egfl7 mutants do not show any obvious phenotypes while animals injected with egfl 7 morpholino (morphants) exhibit severe vascular defects, indicating that the activation of a compensatory network to buffer against deleterious mutations was not observed after translational or transcriptional knockdown.
Journal ArticleDOI

IGF-Binding Proteins: Why Do They Exist and Why Are There So Many?

TL;DR: The emerging explanation that many IGFBP functions have evolved to allow the targeted adjustment of IGF signaling under stressful or irregular conditions, which would likely not be revealed in a standard laboratory setting are explored.
Journal ArticleDOI

Highly Efficient CRISPR-Cas9-Based Methods for Generating Deletion Mutations and F0 Embryos that Lack Gene Function in Zebrafish

TL;DR: Supernumerary guanine nucleotides at the 5' ends of single guide RNAs (sgRNAs) account for diminished CRISPR-Cas9 activity in zebrafish embryos and heritable deletion mutations of at least 50 kbp can be readily induced using pairs of duplex guide RNPs targeted to a single chromosome.
References
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Journal ArticleDOI

Cyclin D2 and the CDK substrate p220NPAT are required for self‐renewal of human embryonic stem cells

TL;DR: While pRB/E2F checkpoint control is relinquished in human ES cells, fidelity of physiological regulation is secured by cyclin D2 dependent activation of the p220NPAT/HiNF‐P mechanism that may explain perpetual proliferation of hES cells without transformation or tumorigenesis.
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FGFR3 Deficiency Causes Multiple Chondroma-like Lesions by Upregulating Hedgehog Signaling.

TL;DR: This is the first study reporting that the loss of Fgfr3 function leads to the formation of chondroma-like lesions via downregulation of MEK/ERK signaling and upregulation of IHH, suggesting that FGFR3 has a tumor suppressor-like function in chondrogenesis.
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Differential roles of cyclin D1 and D3 in pancreatic ductal adenocarcinoma

TL;DR: The results suggest that CCND3 is the primary driver of the cell cycle, in cooperation with CCND1 that integrates extracellular mitogenic signaling and evidence that CC ND1 plays a role in tumor cell migration is presented.
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The nonessentiality of essential genes in yeast provides therapeutic insights into a human disease

TL;DR: Large-scale whole-genome sequencing of essentiality-reversing mutants reveals 14 cases whereby the inactivation of an essential gene is rescued by loss-of-function mutations on another gene, suggesting a loss- of-function therapeutic strategy for the human disorder ADSL deficiency.
Journal ArticleDOI

Normal brain development in importin-alpha5 deficient-mice.

TL;DR: This study showed that mouse embryonic stem cells need to abrogate the expression of importin-α1 and to activate the expression-karyopherinα1 in order to undergo neuronal differentiation in vitro, and indicated that the in vitro findings may be relevant for the in vivo situation.
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