Cells have self-repairing suspension bridges:
Cells face that kind of challenge every day, but they are well equipped to handle it. When both DNA strands break (the “double-stranded break” crisis, or DSB), a cell can die. Molecular machines fly into action as the strands flail about, threatening genomic catastrophe. The repair crew has an additional problem: unlike the bridge cable, the DNA strand is made up of a sequence of code that needs to match what was there before the DSB. In a process called homologous recombination, the machinery searches for a template to rebuild the broken sequence. Researchers at Uppsala University know that this process is mostly “well described in the literature.”
“However, the description usually disregards the daunting task of finding the matching template among all the other genome sequences. The chromosome is a complex structure with several million base pairs of genetic code and it is quite clear that simple diffusion in 3D would not be sufficiently fast by a long shot. But then, how is it done? This has been the mystery of homologous recombination for 50 years. From previous studies, it is clear that the molecule RecA is involved and important in the search process, but, up until now, this has been the limit of our understanding of this process. [Emphasis added.]“
Even a simple bacterium knows a trick to make the search easier. It reduces the search from a 3D problem to a 2D problem. With that shortcut, the cell reduces the time to repair down to 15 minutes on average. The Uppsala group, using CRISPR and fluorescent tags, watched the RecA proteins in real time. They published their findings in Nature.Evolution News, “Tricks of the Cell Trade” at Evolution News and Science Today (September 27, 2021)
After a while, you know it all didn’t “just happen” and the Voice of Science isn;t helping much by claiming that that must beso.