When you eat, you’re basically just taking the useful chemicals from your environment and building yourself out of them. So when a protocell has amino acids and ribonucleotides passing in and out of its cell membrane which it then uses to make proteins and make copies of its nucleic acid, it’s literally just eating the chemical soup that it’s swimming in.
It’s not doing it consciously or deliberately. These molecules are just following the rules of chemistry. Think of it this way: if you have a lot of molecules outside a permeable membrane and only a few inside, as they all move around and cross this membrane, some will leave, some will enter, but there’s a higher chance that they’ll enter than that they’ll leave, just because there’s a higher concentration of molecules outside (at least until it reaches equilibrium). This is known as a concentration gradient.
Now imagine that you have larger molecules that are trapped inside a vesicle or that smaller molecules bond together inside of it and become too big to cross through the membrane – and these molecules have a non-neutral charge. Normally, the smaller atoms and molecules passing in and out of the vesicle would eventually reach an evenly distributed equilibrium, but if they had a positive or negative charge, they’ll either be attracted into or repelled out of the vesicle because of this difference in charge which is known as an electrical gradient.
There’s no magic. No conscious intent. Just chemistry.
Now back to food talk!
Scientists at the Luisi Lab found that when they introduced fatty acids to a solution of fatty acid vesicles, the vesicles grew, incorporating the new material into their membranes – kinda like eating food.
Fatty acid membranes are very dynamic and will even exchange fatty acids with nearby vesicles. When they do that, it’s literally like they’re eating part of their neighbor and getting eaten at the same time – although, not deliberately. Again, it’s just following the laws of chemistry. If you have a few billions of these little protocells in a small pond, but they’re all identical, none of them will have a reproductive advantage over the rest. But imagine if one of them could eat its neighbors faster than it got eaten. It would grow, and before long, it would dominate the population.
Protocells with more genetic content inside of them than their neighbors have just such an advantage!
The negatively charged genetic molecules in a protocell attract in positively charge ions which build up pressure on the cell membrane. As a result, they give up fatty acids from their membrane slower than they attract fatty acids from their neighbors which have less genetic content inside them and, subsequently, less internal pressure. In other words, the faster a protocell can build strands of RNA, the faster it can eat its neighbors and the higher it rises on the food chain. Any genetic mutations that increase the speed and efficiency of RNA replication, would be naturally selected for. This is very non-random survival of randomly variable replicators.
When these vesicles get large enough, simple perturbations (similar to waves in a pond) cause them to split.
But they retained their genetic content inside!
While large strands of RNA are confined inside these fatty acid membranes, amino acids, nucleic acids, and other molecules float freely in and out of the cell’s simple, permeable barriers – this would be essential for life on the early earth. Modern cells, however, with phospholipid bilayers, are far less permeable and more selective with what they let in and out, thanks to transport proteins acting kind of like a bouncer at a high end club.
But why on earth would a cell with a fatty acid membrane start incorporating phospholipids? Is there any advantage to this intermediary stage? What evolutionary pressure would lead it down this path? Itay Budin at Harvard University’s Szostak lab discovered that having even just a small amount of phospholipids mixed into a vesicle’s membrane made the structures more stable. They still absorbed fatty acids from neighboring cells at the same rate, but the presence of the phospholipids slowed down the rate that they lost their own fatty acids - leading to cell growth!
A few mutations leading to a simple phospholipid-forming ribozyme, would be a huge evolutionary advantage - leading to a phospholipid-creating arms race between the protocells. The victor would grow by eating the others and soon dominate the population. As these new protocells’ membranes became more saturated with phospholipids, new evolutionary pressures would emerge. With a less permeable membrane, protocells would now be able hang onto their contents easier and pressures would arise to evolve now-advantageous internal metabolisms. Pressures would also arise for transport proteins capable of regulating what gets in and out of the cell.
Bear in mind:
Billions of cells can potentially occupy one small puddle, and these stages of chemical evolution could have easily been occurring all around the globe. Beneficial mutations helped a cell survived, detrimental ones got it eaten or destroyed. But as soon as a mutation occurred that gave a cell a survival advantage, it would quickly spread and take over the population. And the ones that couldn’t adapt would die out. This is literally the definition of natural selection. Now stretch that change and adaptation out over billions of years, and it’s not surprising that life got more complex.
So we now have a basic RNA-containing cell with an advanced phospholipid bilayer membrane containing transport proteins, capable of absorbing nutrients and competing with its neighbors by eating them or getting eaten - creating natural selection pressures to drive the evolution of life on earth. And because RNA replication does tend to be error prone, the rate and amount of change within populations would lead to very rapid divergence. But can it get us all the way to complex eukaryotes? In my next video, we’ll explore how this simple prokaryotic cell can obtain membrane-bound organelles like mitochondria and plastids.
It kinda blew my mind when I first learned how this happens, so make sure you join my mailing list to make sure you get notified. I've got some cool gifts for you in there when you do.
Till next time, dare to be curious, but don’t drink the Koolaid!
- Chen IA, Roberts RW, Szostak JW - The emergence of competition between model protocells: https://labs.chem.ucsb.edu/chen/irene/Chen_lab_at_UCSB/Publications_files/Chen_Roberts_Szostak_2004_science.pdf
- Itay Budin, Szostak JW - Physical effects underlying the transition from primitive to modern cell membranes: http://www.pnas.org/content/108/13/5249/
- Ting Zhu, Szostak JW - Coupled growth and division of model protocell membranes https://pubs.acs.org/doi/abs/10.1021/ja900919c
- Pier Luigi Luisi, Peter Walde & Thomas Oberholzer- Lipid vesicles as possible intermediates in the origin of life: https://www.colorado.edu/physics/phys7450/phys7450_sp05/downloads/vesiclesoriginoflife.pdf
- Concentration Gradients Explained: https://www.khanacademy.org/science/high-school-biology/hs-energy-and-transport/hs-passive-and-active-transport/v/concentration-gradients
- Electrical Gradient Explained: https://www.youtube.com/watch?v=Ba02v7eoVWQ
- Jack Szostak (Harvard/HHMI) Part 2 - Protocell Membranes: https://youtu.be/CJ5jh33OiOA
- Itay Budin - How do we study the origin of life in the lab?: https://youtu.be/sGzTLyaV29U
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