Answer:
Humans are not that different from other animals, but vary in the finer detail.
Indeed most amniotes (terrestrial organisms with fetuses surrounded by membrane) work pretty well along the same principles, and there’s also much in common as far back as you want to go, really, on land or in water.
And my next semi-random thought is to say that cellular differentiation, like real estate (apparently), is all about location, location, location. Where the cells are, or where they came from, seems to matter a lot.
Actually, it’s more about layers. Like an onion. Or a cake. (I can’t believe I’m writing this, and apologies to any Shrek fans out there.)
What I mean to say is that some understanding of developmental embryology will help here. To simplify things enormously, our adult cell types ultimately arise from embryonic stem cells. These stem cells are multi-purpose and programmable, or pluripotent in a sense, and capable of making whatever type or form of cell is requested. They just need to be “told” what to do. And just tiny bits of code do exactly that, flipping switches on or off as required, based on cues like orientation, chemical gradients, and proximity.
Now a quick read of the links above will explain it all, but I’ll press on anyway. Out of that initial programming arises our ‘germ layers’, the mesoderm, the ectoderm and the endoderm. We are, after all, triploblastic. 3 layers, get it?
But you knew that.
In case you didn’t, these layers in effect give you a scaffold or more accurately perhaps a tube comprising an inside, outside, and a middle. Where your cells are hanging out in that tube matters, in that they pick up on their location and auto-magically become functionally relevant to that space. In a sense, I mean. Refer back to location, location, location.
Just knowing that pattern of proximity, gradients, and orientation more than simply sets the scene. Whether you work forwards or backwards from there, you will hopefully see that these “germ layers” derive quite simply from a much earlier differentiation, and then complexify. In that sense you have your answer - a complex set of diverse cell types arises by differentiation from an earlier, simpler differentiation. Which sounds a bit clunky when I write it out, but it gives a general idea.
So how does this complicated process happen?
Well, as I mentioned chemical gradients are probably to blame here. And it actually starts before fertilisation, in that the egg itself is already semi-structured and bathed in chemicals with a high-low gradient of some sort. In that sense it’s giving cellular differentiation a head start (there’s a pun there), by setting up some sort of polarity from the beginning. At the very least we get some ends happening, or a top and a bottom if you like.
Now, again simplifying things enormously, your average fertilised egg, or zygote, has by definition a complete set of your DNA ready and waiting, which contains the code for every protein-making gene, plus transcription factors, plus whatever else gets copied for various reasons, including those we haven’t teased out as yet.
Note that those transcription factors really matter. We may have around 20,000 protein-expressing genes, but we also have some 1,500 transcription factors that seem to switch the genes on, off, or arguably and effectively somewhere in between. Well, they work in combination and by that we get a huge amount of variation in expression, and thus our cellular diversity as well.
And all of that DNA goodness is sitting in that zygote, bathed in chemicals that may vary very slightly from top to bottom and side to side as it were, by concentration and by other traits, like temperature. Several such things interact, including orientation and proximity to neighbours, but let’s assert (based on experiments) that the gradient is important, and that it continues to guide the “differentiation” process as new cells are born.
Which is to say that by this process of reading the DNA and expressing only the genes that are switched on by the helpful and gradient-sensitive (say) transcription factors, we get set up to form those 3-D axes and the scaffolding that will guide our cellular replication strategy. Which then produces a result that with each round of replication becomes subtly different and more diverse. Over time the subtlety gives way to more recognisable layers and specialisation in function.
Perhaps not the neatest, clearest explanation but the quickest and least baffling one I can come up with right now. As always, read the links to get a better grasp.
