In the beginning there was an acidic ocean, alkaline hydrothermal fluid and a precipitated Fe/Ni sulphide catalytic interface.
You can do this in a bench top reactor which simulates such conditions, a modern version of the Miller Urey experiments from the 1950s. The atmosphere is 98%nitrogen with 2% hydrogen. It's strictly anoxic. The FeCl2, NiCl2 and Na2S in the perfusates are at millimolar concentrations and the yield of formic acid is in the region of 50 micromol/l, sampled in the fluid close to the precipitated Fe/NiS tubes. The equipment looks like this:
That, to me, is a pretty good start. The full paper is here and can be downloaded for free.
Below is what the reactor is simulating and what it is probably doing. It's a simplified reaction pathway compared to the one I talked about back in February. It doesn't supply a HS-CH3 source so generates formate rather than acetate:
The pH gradient across the FeS layer generates a reduced FeS moiety:
Reduced FeS provides the conditions for hydrogen to reduce carbon dioxide to carbon monoxide:
Carbon monoxide reacts with hydrogen to give formaldehyde and formic acid:
This much can be demonstrated on the bench top. It relies on far-from-equilibrium conditions modelled on those found at alkaline hydrothermal vents. These vent systems are not volcanic in origin, they are generated by the conversion of olivine to serpentine by water and are stable over geological time scales. This is a source of carbon, produced on a continuous basis, which can react further to give many organic compounds essential to life. No further energy input is required.
The next step needs us to get much more speculative and to consider the situation in a microporous FeS structure like the one fossilised at Tynagh in Ireland.
Imagine that we have a porous honeycomb of FeS which allows protons from the ocean to combine with hydroxyl ions from the vent fluid within a hollow vesicle. This neutralisation of protons allows continuous flow of more protons in to the protocell.
As protons pass in to the vesicle they continue to provide a source of reduced FeS which drives the reduction of CO2 in to assorted prebiotic chemicals, lumped together here as "metabolism":
Sufficient "metabolism" could plausibly produce a lining of assorted organic compounds, here described as "crud". Forming a protomembrane which is somewhat impermeable to Na+ is relatively simple. Making one proton-proof (or hydroxyl proof) is far more difficult:
Once we have a protomembrane which is opaque to Na+ ions we have the possibility of a Na+/H+ anti porter using the continued passage of H+:
I don't see the need for an antiporter to be specifically generating a Na+ ion gradient per se, pumping a few Na+ ions out of a cell will not alter the Na+ ion concentration outside the protomembrane. This is "locked" at the Na+ concentration of the ocean. No, all we need is some functional benefit from having a lower Na+ level within the protocell and there is then a benefit from Na+ expulsion. That might be because the residual Mg2+ and K+ are more effective for catalysis of the on-going nascent biochemistry with lower Na+ concentrations. So the Na+ gradient is generated by a reduced intracellular Na+ concentration. It can be maintained by a Na+ opaque membrane which is still proton permeable:
However, once it is there, the gradient becomes a source of useful potential in its own right. Recall that ATP synthase probably started as an ATP consuming, sodium extruding, modified protein translocase. It is very plausible that this initial usage of ATP to lower intracellular Na+ as a supplement to the anti porter. When the vent fluids are providing Na+ lowering for free, the lowered intracellular Na+ level makes it increasing difficulty for ATP synthase to further expel Na+ ions and provides an increasing pressure for it to run in reverse and convert the Na+ gradient in to ATP, especially under conditions reduced availability of ATP. This gives bulk ATP production coupled indirectly to the H+ gradient of the vent via a biologically generated Na+ gradient across a relatively non sophisticated membrane.
[The more I think about this the more ATP synthase may well have been acting as a Na+ pump BEFORE the Na+/H+ anti porter developed, i.e. a reduced intracellular Na+ was being paid for with ATP from substrate level phosphorylation via acetyl phosphate derivatives until the anti porter developed. The anti ported suddenly out stripped ATP synthase's ability to expel Na+, did it for free so long as the vent fluid was there, and so could reverse ATP synthase to make an actual synthase rather than a consumer of ATP. Makes sense, to me anyway].
For a cell to leave the proton gradient provided by the hydrothermal vent it must continue to expel Na+ without assistance from said proton gradient. This problem was solved in the same way by the archaea and the bacteria but using different techniques, i.e. it is unlikely to have been a core process in LUCA. Both techniques are based around electron bifurcation:
Hyd stands for soluble hydrogenase and Hdr is heterosulphide reductase. These take H2 and split the pair of electrons available. One electron goes steeply down-potential and the free energy of this reaction is coupled to getting the second electron to a potential where it can manage the generation of the reduced FeS which was originally provided by the proton gradient. Ferredoxin is a very primordial FeS containing protein. It stores low potential electrons on an FeS group and moves them around to places where they are needed. To a Na+ ion pump for one.
Electron bifurcation replaces proton gradient derived reduced FeS with biochemically derived reduced ferredoxin. Given sources of H2 and CO2 a cell is then potentially independent of the vent conditions:
From previous posts the archaeal and bacterial lineages have already divided before leaving the vents. The technique for electron bifurcation is different and the locking mechanism for ATP synthase is also different. The problems are the same, the solutions are clearly related but not quite identical. We can overlay this set of ideas on to the metabolism of modern Na+ pumping methanogens and acetogens by modifying the diagrams from Sousa et al's Early bioenergetic evolution.
First the acetogen:
This is the basic plan of bioenergetics in a Na+ pumping acetogen. If we highlight the core reactions of activated acetate formation we have reduced ferredoxin converting CO2 to CO (using H2, omitted for clarity) and combining with HS-CH3 to give a precursor to acetyl phosphate:
As an alternative to providing ATP the acetyl phosphate can be diverted to cell carbon synthesis:
The soluble hydrogenase (Hyd) is using electron bifurcation to generate the Fd- to drive the reduction of CO2, replacing the vent proton gradient. This Fd- is also being used to drive Na+ expulsion via Rnf, a Na+/H+ antiporter modified to use Fd- to replace the proton gradient. Rnf is the ancient ancestor of complex I. Complex I still carries the anti porter component of Rnf.
So in acetogens both carbon fixation and Na+ pumping are driven by electron bifurcation which replaces the vent proton gradient. What about methanogens? Here we go, this is the basic plan:
[I've not bothered correcting the small typo in Sousa's diagram].
So, the first thing we have to draw in is the components of the acetyl phosphate generating limb. This was omitted from the original diagram as it is only used for carbon fixation, not Na+ pumping or ATP synthesis. Note that ATP synthesis is now based on ATP synthase, not acetyl phosphate derived substrate level phosphorylation:
So let's overlay the primordial CO2 fixation pathway again:
In methanogens electron bifurcation is carried out by heterodisulphide reductase (Hdr) which is supplying a reduced Fd- pool to the cell to drive CO2 reduction as before:
but the Fd- pool also supplies the electrons to reduce CO2 to
CHO-MFR down to the Methyl-H4MPT, which I have over written with HS-CH3:
This pathway is a modern cofactor stabilised version of Nick Lane's bench top reactor driven formaldehyde formation. It goes like this:
CHO-MF is formaldehyde safely stored on the cofactor MFR.
CHO-H4MPT is simply a change of the cofactor used for storing the formaldehyde (formyl-H4MPT).
Removal of the oxygen atom of CHO reduces the formaldehyde to a CH moiety triple bonded to the cofactor (methenyl-H4MPT).
More reduction gives CH2 double bonded to the cofactor (methylene-H4MPT).
Next reduction gives a methyl group attached to the cofactor.
This (CH3-H4MPT) is over written by the HS-CH3 in the diagram as they are doing essentially the same job.
This methyl donor can be used for carbon fixation via acetyl phosphate or to drive Na+ expulsion via the MtrA-H complex. The later is probably based around the same Na+/H+ anti porter as Rnf but has a different module, methyl derivative powered, added to replace the proton gradient.
We can follow through from the very basic acetyl phosphate pathway, plus a Na+/H+ anti porter, plus a power source to replace the H+ gradient component of the anti porter, plus an ATP synthase, to give us a picture of the pathways giving rise to those acetogens and methanogens which have developed the origin of life pathways to highly sophisticated modern derivatives but with minimal changes to the general principles.
This is the logical picture which other origin of life scenarios are up against. I like simple logic. I like this hypothesis. It may be incorrect, but I hope not.