Neurons migrating through dense tissue in the developing brain (green) frequently undergo DNA damage (magenta).
Like my last post, this post illustrates how the human body, far from being the perfect design of the omnipotent, omniscient designer creationists would have us believe in, is the result of a utilitarian evolutionary process. Layers of complexity arise, not from divine brilliance, but from evolved solutions to problems created by suboptimal earlier solutions to other problems — which were themselves the result of imperfect evolution.
In the previous post we saw how DNA replication is sufficiently imperfect that it requires mechanisms to repair the resulting DNA damage. However, these repair processes are themselves potentially dangerous and need control systems to maintain a careful balance between too little and too much repair. When this control process fails, it can lead to cancers that mimic those caused by the BRCA1 and BRCA2 genes, which are associated with increased risk of breast and ovarian cancer.
In this post we see how newborn neurons in the developing brain need to squeeze through tight spaces in dense tissue, past other cells and between fibres, in order to reach their final positions and form neural circuits in the cerebral and cerebellar cortices. This process is such a physical struggle that the DNA in these neurons can suffer double-strand breaks and must be repaired quickly to ensure normal brain development. This is the finding of a research team from Kyoto University, the University of Tokyo, Osaka University, the National University of Singapore and the Tokyo Metropolitan Institute of Medical Science, led by Professor Mineko Kengaku who have just published their findings in Nature.
Mostly, this repair is quick and successful. However, the research team also found striking similarities between the development of mice in which the repair process failed and human genome-instability syndromes that affect the cerebellum.
Another important point is that this repair process appears to be much more successful in damaged neuronal DNA than in similar damage that can occur when some cancer cells migrate through narrow channels. The difference seems to lie in where the DNA breaks occur. In neurons, they tend to occur in regions of the genome that are not actively being transcribed, whereas in cancer cells the damage can involve essential genes. That suggests there is some biological bias in where these breaks occur in neurons, rather than the process being simply random mechanical shattering.
This raises the obvious question for creationists: why create a process that breaks DNA in developing brain cells, only to require another process to repair it, with the inherent risk that the repair process might be incomplete or imperfect? It also raises the possibility that the resulting small differences in the genomes of individual neurons could contribute to neuronal individuality and perhaps to some neurodevelopmental or neurodegenerative diseases.
The emerging picture, from this and from the rogue repair-control process that can mimic cancers caused by the BRCA genes, is not of a human body designed by an omniscient engineer. It is more like a William Heath Robinson contraption: improvised, overcomplicated, dependent on compensatory mechanisms, and always vulnerable to the failure of the very systems needed to keep it working.





























