We already looked at vent 1, now onto vent 2.

Vent 2 has two populations: anae2 and anae6.  Now, remember, anae2 was the offspring of an individual of anae1 that had a mutation in an enzyme responsible for energy production. Anae6 is anae2#101 (random individual in the population) with a mutation in the other enzyme. Because of this, anae6 is not as efficient at energy metabolism and takes twice as long to divide as individuals in the anae2 population.

 We're in familar territory here, and a number of directions are possible for these two populations competing for resources at the vent. But let's ignore the details and get down to possible mutation directions.

Possible changes in offspring due to polymerase infidelity(otherwise known as copy errors when the DNA is copied for the cell division - not all inclusive, it would be nearly impossible to predict everything nature can do):

1) Anything similar to what was seen in the other populations we've already discussed, but they can occur in other genes.

• Let's say, like anae5, but the organism loses pigment (anae9).

•  Like anae 7 and 8, a surface protein has an amino acid shift that allows it to be extracellular and bind to others with it, but it's a protein that is not complementary to the one mutated in 7 and 8 and cannot bind them (anae10). Or it can be a different, but complementary protein and can bind them (anae11).

2) Something we haven't seen before - the signal sequence on an intracellular protein is mutated and is now secreted. What the protein does will determine the effect this mutation has.

• The protein is essential to cellular function - the cell will die immediately the mutation is gone as well
• The cell has a redundant protein to cover for the missing one - the cell continues life normally, passing on the mutation and secreting the protein. What this protein can do once secreted will determine the effect. Will it bind to the outside of other cells (hormone)? Will it attract predators? Will it do nothing? (anae12)
• It is a structural protein not necessary to division or cellular metabolism - the cell may lose mobility, may lose shape, and the protein may have effects once secreted.  

As you can see, we have 4 new populations. They could stem from a replicative error of either anae2 or anae6. They are likely unrelated to the already present mutations (though they could be). For simplicity let's take them all from anae2.

Now, the mutation in anae6 likely produces splice variants, which is why the enzyme still functions. Some of the enzyme produced is functional, some isn't. But that doesn't mean they have no function at all, just not what it is expected to. Let's say that there are three splice variants: short, long, and merged. The long variant is the original, functional enzyme. The short variant is quickly degraded by the cell. But the merged has enough sequence to not be degraded, but it isn't functional as the original enzyme. Instead, it is capable of binding DNA.When it binds DNA, it stops the transcription and replication machinery. We now have a negative regulatory transcription factor and a number of genes just got shut off. 

If the genes control cell metabolism, the cell dies and anae6 doesn't survive beyond that one. If the genes have more subtle roles...well, this is where it gets real interesting real fast.