Transcriptome analysis in alleles displaying mutant mRNA decay reveals the upregulation of a substantial proportion of the genes that exhibit sequence similarity with the mutated gene’s mRNA, suggesting a sequence-dependent mechanism. These findings have implications for our understanding of disease-causing mutations, and will help in the design of mutant alleles with minimal transcriptional adaptation-derived compensation.
We show that upf3a (a member of the nonsense-mediated mRNA decay pathway) and components of the COMPASS complex including wdr5 function in GCR [the genetic compensation response].
Reported as: Genetic paradox explained by nonsense 4/3/19
Gene mutations that truncate the encoded protein can trigger the expression of related genes. The discovery of this compensatory response changes how we think about genetic studies in humans and model organisms.
Who hasn’t placed this into the context of the light-activated assembly of the microRNA-RNA-peptide
nanocomplex and linked biophysically constrained viral latency from autophagy to DNA repair in all living genera via the physiology of reproduction?
See: All About that Base 12/10/14
Codon identity is energy-dependent. The energy biophyiscally constrains viral latency in the context of the physiology pheromone-controlled reproduction in species from microbes to humans.