Cell-type differentiation

By: James V. Kohl | Published on: February 7, 2014

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How Do You Know When You’ve Found Them All? A Question That Applies To Beetles and Cancer Genes Alike

by Carl Zimmer
Conclusion: “Cancer biologists and beetle experts are not all that different when you think about it. They walk the same foggy road together, a long way from the end.”
My comment: Only the cancer biologists and beetle experts who believe in mutation-driven evolution are walking a road together. It’s not a foggy road. It’s brain fog that makes them similar. Serious scientists have long since realized that the molecular mechanisms of cell type differentiation must be considered to make scientific progress based on experimental evidence that has replaced pseudoscientific theory. That’s why serious scientists are not far from the end of the road, which is when models that incorporate the atoms to ecosystems perspective are examined without the fog of theory.
See for review: The dsRBP and Inactive Editor ADR-1 Utilizes dsRNA Binding to Regulate A-to-I RNA Editing across the C. elegans Transcriptome.
In the model organism C. elegans, Adenosine deaminases that act on RNA (ADARs) cause changes in the molecular building blocks of RNA. Adenosine-to-inosine editing (A-to-I editing) diversifies genetic information that specifies the different amino acids, splice sites and structures that stabilize the organized genome. Levels of ADAR proteins are not altered in disease.
That fact and other biological facts tell us that perturbed molecular mechanisms of protein folding are involved in diseases but not in organization of genome-wide stability of cell types in species from microbes to man. Clearly, there are differences in molecular mechanisms of diseases and regulated ADAR-mediated RNA editing. We can expect that ADAR-mediated RNA editing involves the nutrient-dependent pheromone-controlled microRNA/messenger RNA (mRNA) balance and alternative splicings of pre-mRNA for example.
If not for the ridiculous theory of mutation-driven evolution, cancer biologists and beetle experts could be working without the fog. They would be looking at the nutrient-dependent pheromone-controlled microRNA/mRNA balance. That would bring them closer to learning the difference between mutations and ecological adaptations that lead to increasing organismal complexity via alternative splicings of pre-mRNA and de novo gene creation.
They could compare their works to what they already know about mutations and disease. The comparisons would be enlightening.
Everyone knows that nothing about the systems biology of cell-type differentiation makes sense except in the light of ecological adaptations. Cancer biologists and beetle experts would present their experimental results in the context of ecological adaptations that could be compared to mutations associated with diseases and disorders. Both brain-fogged groups would abandon the idea of mutation-initiated natural selection. They would understand the difference between the role of mutation in disease and the role of ecological adaptations in health.
See also: Docosahexaenoic Acid: A Potential Modulator of Brain Tumors and Metastasis and Regulation of pre-mRNA Alternative Splicing by the RNA Processing Factor hnRNPL