Comment by randomImmigrant

The author cops to teleology, apologizes for it, then continues to use it to explain these behaviors.

This is always a problem when one tries to view biology through an engineering lens. The functions we see today emerged well after the genes themselves started on the path that allowed them to support these specific functions in us. Nor are the genes restricted to exactly identical functions even when their sequence is identical. The context of each cell matters.

Rather than beginning from external function and going down to find energy, replication and cancer/escape from multicellularity as factors affecting these organ’s behavior, it’s a lot better to go cell up, where metabolism, DNA replication, waste clearance, and cell to cell communication and cell-microenvironment sensing are all constantly having to be balanced.

The functions we see from ensembles of cells are composed of these cell level behaviors multiplexing.

And when we look at the eukaryotic cell, we don’t just see linear DNA. We also see mitochondria. Our mitochondria reproduce and proliferate in all cells, depending on energy requirements. The process also produces a lot of reactive oxygen species which need to be kept tamped down to prevent damage.

And the mitochondrial endosymbiotic event also potentially explains why we have linear DNA in a separate compartment. From first eukaryotic common ancestor (FECA) to the last eukaryotic common ancestor (LECA), you had two genomes inside one cell, and by the time we got to LECA a bunch of DNA from the alphaproteobacter that became mitochondria migrated to the core genome, leaving the mitochondrial genome to remain circular.

The exact time and reason for linearization of DNA is (as yet) lost to deep time. But we can see a path from two circular genomes to one linear one circular and construct a fairly believable hypothesis to why you got linearization: as cell type increased, you needed more transcript copies, and access to different transcripts at different times at different rates. A linear genome is much better able to accommodate these requirements. And this has resulted in prokaryotes also partially or fully linearizing some of their genomic material when the need arises (Cyanobacteria, the first autotrophs, have some strains with linear ends, and Lyme disease and streptococcus also break from full circularity).

This linearization is also critical for mitosis and meiosis.

As far as the exact causal chain, we are, at the moment, groping in the blind, since the FECA->LECA transition occurred some 2 billion years ago, and we don’t have candidate fossils. They are reconstructed from genomic puzzle pieces, which is why we have these holes.

In that transition timetable, it is possible commitments were made that shape everything we see today.

Beyond doubt, those commitments had to thread everything a single cell has to thread.

And then came multicellularity, which had its own tradeoffs.

Teleology doesn’t help because none of these early commitments were being made with the specifics of our current lifestyle in mind, or even that complex beings like us could exist.

Evolution is a blind watchmaker. Ignore that and you’ll end up with nice sounding ideas that may not quite fit what we see.