So in that sense, a global maxima (minima?) solving function will probably not arrive at what we have, it has to take into account our evolutionary path, in its entirety (as in the whole tree.), because it is all encoded in 1 (or several) long molecules, and a radical changes would take a rewrite of many parts at the same time, which just does not happen. Maybe at some point we can do it ourselves... though I imagine there being a lot of unintended consequences in other places in the body :).
Another example is that sometimes complexity in a cell signalling cascade is simply there to get some timing right (ie delay some response), and the complexity is just there, and won't simplify by itself -> But then later the complexity may start to serve some purpose. Just like proteins that are "copypasta-ed" in the genome, leaving one copy free to mutate and attain a function, or not... etc etc.
https://futurism.com/evolutianary-proof-the-recurrent-laryng...
I did not know human urinary tract was suboptimal.
Are there examples of "discontinuous" evolution where a chance mutation stumbled upon a much better way to do something that allowed a species to jump the gap?
I imagine it would be very rare because chance mutations in a single individual that confer extraordinary survival / mating advantage to offset entire population would be rare like being a superman among men.
But you were probably asking for multicellular eukaryote organism; you may be interested in the concept of saltation https://en.wikipedia.org/wiki/Saltation_(biology) . Behind the concept of the thing itself it's interesting to think about the mechanism behind it. Regular evolution is gradual (point mutation leads to a maybe slightly different protein, which has only a relatively small scale effect but you gain or lose function over many generation), but for a saltatory evolution you most probably need radical changes in the DNA, like duplication (of a single gene, multiple gene or whole chromosome), horizontal exchanges, etc.
It's possible in plant but in animal more often than not it's not beneficial at all to have such event. Famously if you have an extra chromosome nr. 21 you get Down syndrome.
-> This also depends on population size, if there is a bottleneck event (ie 99.99 percent of some species dying) then among the 100's of survivors perhaps there could be a superman. Either because this person got lucky, or the rest got unlucky. But in general the distribution of traits is quite continuous, given large populations.
It's also good to keep in mind that us biologists have messy definitions, ie we call specimen A and B the same species when they produce fertile offspring. Some species produce offspring but infertile (Horse-Donkey, Lion-Tiger). But what if A and B have fertile offspring and B and C do, but A and C do not? The whole definition of species falls apart (it leads to a paradox).
We have a lot of that in biology. You need to learn to deal with it (sunglasses dropping down), and assign uncertainties to terms you learn about, they are often just our attempts to name boxes on continuous, multidimensional scales.
As for "discontinuous evolution"... Again, what is discontinuous? I'm sure there are events to be found of which the probability of them occurring is so small and the effects so large that they'd fall into someone's definition of "discontinuous". But I think there is by definition no such thing as discontinuous evolution. If it occurred, it had a non-0 probability of occurring, then again, maybe the universe is infinite and everything has a non-zero probability of occurring. This is getting philosophical haha. Maybe listen to some Mindscape podcasts (Sean Caroll).
Actually rabbits eat their excrement again. That's also probably not how an engineer would make it (or an intelligent designer would design it, since we seems to be going in that direction ;) ).
a suboptimal trait evolving that still provided an overall population benefit (via survival or reproduction) with further improvement close to impossible without a multitude of large changes is literally just a local maximum in that high dimensional space that maps traits to whatever success metric you're measuring.
the infinite wall you describe is not a wall in that space. actually I originally wrote its more like a wall in the derivative space but its not quite right either, those just point straight down from the maximum.
So, it's a bit context dependent, and definitely dependent on other mutations that have occurred in other parts of your DNA. Most complex diseases are "polygenic", meaning it's a culmination of quite a few factors that would contribute to a specific good or bad outcome.
So, yes, it could be modeled as a sort very context dependent with a lot of highly correlated non-independent covariates. We do use quite a lot of statistical and ML methods to understand the genome (I work in statistical genetics), but the complexity of biology has so far proved a tough nut to crack.
Survival rate/reproduction rate/rate of genes being spread?
see thrify gene hypothesis; I know it's not a good explanatory theory but it's a good illustration of my point