For years, I have been trying to flesh out the conceptualization of front-loading evolution at the origin of life. A working hypothesis has been that the first cells (uni-cellular life forms) were front-loaded with information that would facilitate the evolution of multi-cellular life. One possible candidate for such front-loaded ‘information’ would be the homeodomain proteins. These proteins play essential roles in metazoan development and are considered part of the developmental toolkit as outlined by biologist Sean Carroll.

A few months ago, a study was published that outlines data and arguments that perfectly resonate with my front-loading views. Let’s have a look.

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I mentioned before that RecA was a motor protein . Well, recent data confirm this. :

Additional biophysical and biochemical analyses revealed that RecA family proteins may couple ATP binding and hydrolysis to the DNA strand exchange reaction in a manner that promotes clockwise axial rotation of nucleoprotein filaments. Specially, the 61 RadA helical filament undergoes clockwise axial rotation in 2 discrete 120° steps to the 31 extended right-handed filament and then to the 43 left-handed filament. As a result, all the DNA-binding motifs (denoted L1, L2 and HhH) in the RadA proteins move concurrently to mediate DNA binding, homology pairing, and strand exchange, respectively. Therefore, the energy of ATP is used to rotate not only DNA substrates but also the RecA family protein filaments.

That RecA would function like this is suggestive of common design. For example, the RecA protein belongs to the same family as the beta-subunits of the F-ATPase. More on this some time in the future.

Even more music for the Matrix

More music for the Matrix

According to Mats Ljungman, a researcher at the University of Michigan Medical School, as many as 20,000 lesions occur daily in a cell’s DNA. To repair all this continual damage, how does the cell first detect it? Ljungman’s research identified the logical candidate – RNA polymerase (the machine that reads the DNA and makes an RNA copy). Apparently, whenever the RNA polymerase encounters a lesion, it signals to p53, a master protein that activates all sorts of DNA repair processes.

According to the press release:

“These two proteins are saying, ‘Transcription has stopped,’” says Ljungman. These early triggers act like the citizen who smells smoke and sounds a fire alarm, alerting the fire department. Then p53, like a team of fire fighters, arrives and evaluates what to do. To reduce the chance of harmful mutations that may result from DNA damage, p53 may kill cells or stop them temporarily from dividing, so that there is time for DNA repair.

Recently, the ENCODE consortium determined that the majority of DNA in the human genome is transcribed:

This broad pattern of transcription challenges the long-standing view that the human genome consists of a relatively small set of discrete genes, along with a vast amount of so-called junk DNA that is not biologically active.

Of course, one could also argue that all this transcription simply speaks to the sloppy and wasteful nature of the cell. Yet here’s a thought. It would seem to me that Ljungman’s research now raises a third possibility: all that transcription is just another layer of error surveillance.

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