Adaptations to stress encourage mutations in a DNA area that causes diseases

This 2015 Baylor study of human cells showed the underlying mechanisms of cellular responses to environmental stressors of cold, heat, hypoxia, and oxidation:

“Because trinucleotide repeats are overrepresented in gene-regulatory proteins, stress-induced trinucleotide repeat mutagenesis may provide a path for the environment to subtly alter gene regulatory networks—with attendant changes in cell behavior—during development, disease, and evolution.”

The study’s overarching framework was that human cells will adapt to best survive in their environment. The study found that the cells’ adaptation responses to stress encouraged the creation of mutations in a DNA area that’s:

“..the cause of multiple human diseases.

This pathway may impact normal cells as they encounter stresses in their environment or during development or abnormal cells as they evolve metastatic potential.”

It’s a logical inference to likewise understand how stressors in a mother’s environment for a developing fetus will cause the fetus to adapt at the cellular level. If, for example, the mother stresses the fetus with inadequate oxygen – hypoxia – this study shows how cells will adapt in a way that favors genetic processes and mutations to survive when they are starved of oxygen.

When the stressed fetus arrives in a different environment after birth, the newborn’s cells are genetically and behaviorally maladapted to certain aspects of a normal environment – to adequate oxygen in this example. The genetic pathways epigenetically adapted to best survive during the fetus’ development in the womb may begin to impact the infant’s development in a normal environment.

Researchers would make significant contributions to the existing science should they further investigate these stress-induced underlying causes. “Environmental stress induces trinucleotide repeat mutagenesis in human cells”


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