CRISPR Corrects Blood Disorder Gene
Scientists use the genome-editing technique to fix a disease-causing mutation in human cell lines.
| August 5, 2014
Excerpt 1): “β-thalassemia is caused by a mutation in the HBBgene, resulting in a severe hemoglobin deficiency.”
Excerpt 2): “One of the concerns with using CRISPR is that it has the potential to snip other, unintended sites in the genome.”
My comment: My concerns about using CRISPR are based on the likelihood that β-thalassemia results from nutrient-dependent amino acid substitutions that stabilize DNA in organized genomes. If so, using CRISPR will lead to genomic instability akin to using pharmaceuticals that alter protein folding and cell type differentiation that is nutrient-dependent and pheromone-controlled.
My comment to The Scientist appears below:
Excerpts from: Detection of hemoglobinopathies and thalassemias using automated separation systems
1) “The hemoglobinopathies, or Hb variants, are attributable to amino acid substitution(s) in either globin chain. Currently, 1,179 total hemoglobin variants have been characterized.2”
2)”Countries with the highest incidence of diabetes also tend to have high incidence of Hb variants in the population.14″
Correlations (don’t say it*) between amino acid substitutions that appear to differentiate the cell types of all cells in all individuals of all different species suggest the amino acid substitutions that differentiate cell types with hemoglobin variants and those that somehow contribute to diabetes also are nutrient-dependent.
However, the amino acid substitutions are not likely to become fixed in the absence of their effect on DNA stability in the organized genomes of species with circulatory systems that also produce pheromones, which control the physiology of reproduction in species from microbes to man.
For examples of other correlations in species with and without circulatory systems see: Nutrient-dependent/pheromone-controlled adaptive evolution: a model.
Is there a model of mutation-caused cell type differentiation via amino acid substitutions in species from yeasts to mammals? If not, my model may be the only model of biophysically-constrained biologically-based cause and effect that can be compared to correlations provided in the context of theories about how mutations and natural selection somehow led to the evolution of biodiversity.
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* Don’t say that correlations are not causation unless you first attest to the fact that you have never thought in terms of Mutation-driven evolution without recognizing your unstated belief that correlations must be causation. If not, the theories about mutaitions are not biologically plausible theories.
