About this Research Topic
It has been broadly appreciated that genetic robustness plays an important role in living organisms’ viability, fitness, and adaptation to genetic and environmental perturbations.
However, the underlying mechanisms of how organisms use the ability of genetic robustness are complex and require further investigation. Since reverse genetic tools such as CRISPR, morpholino, and siRNA, have started to be used for experimental investigation of gene function, we have obtained straightforward approaches to finding the potential roles of the gene of interest in various model organisms. A growing number of studies unveiled the inconsistencies observed between phenotypes obtained from mutant and knockdown approaches due to genetic compensations, rather than off-target effects.
Recent investigations uncovered some of the underlying mechanisms involved in genetic compensation response (GCR), including nonsense-mediated mRNA decay, however, further research on these mechanisms is still needed.
The large majority of GCR studies are conducted in Zebrafish models, but similar discrepancies are also reported in other model organisms including mouse, Drosophila, yeast, and Arabidopsis, indicating, that GCR is likely conserved across species.
In this Research Topic, we aim to further understand phenotype discrepancies between knockout and knockdown approaches, have a comprehensive catalog of refined gene functions during embryonic development, and elucidate the molecular mechanisms behind genetic compensation and how they affect the embryonic development process both in animal models and organoids.
We would like to discuss and clarify:
- Whether the phenotypes are reflecting the authentic function of the gene of interest.
- Phenotypic variability related to the use of different gene knockout and knockdown approaches, also considering differences in developmental stages, tissue, and experimental setup in model animals or organoid systems.
Areas to be covered in this Research Topic may include, but are not limited to:
• Studies reporting genetic compensation in model animals and outlining possible molecular mechanisms.
• Studies reporting genetic alteration effects on organoids and their possible reflection/discrepancies in in vivo systems.
• New or systematic screening methods/approaches to discriminate between off-target and authentic phenotypes derived by gene knockdown.
• Gene expression analyses during embryonic development caused by genetic compensation of the gene of interest and relative molecular mechanisms.
We welcome different article types including Original Research, Reviews and Mini-Reviews, Methods, Brief Research Reports, and Perspectives. A full list of accepted article types, including descriptions, can be found at this link.
Keywords: Genetic Compensation, Genetic Robustness, Gene Function, Embryonic Development, Organoids, Animal Models, Knockout, Knockdown
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.