The Pioneers: Archaea and Bacteria

phylogenetic tree wikipedia

Animals and Plants, in the upper right corner, no longer headline the Tree of Life.         (Wikipedia)

The most basic categories of living things are not what they used to be. In the past they included Plants and Animals, but no longer. Today the three Domains are all named for organisms too small to see. Plants and Animals, including humans, have become small print within a Domain called Eukaryotes (you-CARRY-oats), meaning cells with a nucleus.

A second Domain is Bacteria. The third is the Archaea. Not sure how to pronounce Archaea? I wasn’t either. It’s AR-kee-ah or ar-KY-a; both are acceptable. That noun is plural; the singular is AR-kee-on, an Archaeon, sounding faintly of Star Wars.

Archaea are like Bacteria in that they have no nucleus and are simpler, smaller and older than Eukaryote cells. So how are these Archaea so different from Bacteria that they get their own Domain? Biologist Carl Woese in 1977 argued successfully they are indeed a different form of life. I’ll describe a few features that Archaea and Bacteria have in common and then others that seem unique to Archaea.

Both Archaea and Bacteria are small, unstructured, and simple compared to the Eukaryotes that evolved. But one achievement they both share has been to try out nearly every possible chemical or environmental source to get their energy. Sunshine, salty water, temperatures ranging from volcanic to polar, even radioactive settings—varieties of Bacteria and especially Archaea have found ways to draw energy from, and live off of, these and other environments.

Another similarity is that Archaea and Bacteria don’t reproduce sexually; two cells don’t mingle their genes to form a new individual. Instead, individual cells just multiply their insides by two and then divide to form identical daughter cells. To put some variety into their DNA, they both use a technique other than reproduction. A Bacterium or Archaeon can pump some of its DNA into another cell. Or a cell can just pick up a bit of DNA floating near it. No merging, just some sharing. This gene-sharing is called lateral gene transfer. It is important to know about.

archaea hot springs yellowstone nationa park (

Archaea at home in a Yellowstone hot spring.       (

For starters, gene sharing is one reason that antibiotic-resistant bacteria in hospitals can spread their immunity to other bacteria so quickly. And gene sharing  doesn’t have to take place between members of the same species, as sexual reproduction usually does. Instead, DNA can be transferred from any species of Bacterium or Archaeon to any other species within the same Domain if the conditions are right.

If plants and animals could carry on such gene swapping, the mind boggles. Squirrels could transfer some of their DNA over to dandelions. Or vice-versa. Such promiscuity helps explain how Bacteria and Archaea have evolved so many different ways to live in extreme environments, as well as so many different colors.

But Archaea are also distinct from Bacteria in notable ways:

  • Archaea were first discovered in extreme settings where even Bacteria fear to tread: geysers, intensely salty water, even thermal vents at 251 degrees F, the hottest place any organism has been found living.
  • Another feature is that, while some varieties of both Archaea and Bacteria get their energy from light, Archaea do it their own way, through a process unrelated to the photosynthesis going on around us in plants. Importantly, too, only Archaea produce methane, essential to organic decomposition.
  • Finally, while many Bacteria can make us sick—Lyme, Cholera, Syphilis—Archaea may be nicer: No pathogenic Archaea have been discovered––so far.

Archaea and Bacteria had the Earth to themselves for over a billion years. Then about two billion years ago, Eukaryotes appeared, evolving from their single-celled predecessor but larger and internally more developed. By then, Archaea, like Bacteria, had carried out much of the groundwork for living, pioneering what it takes to survive in different conditions, experimenting with energy sources, trying out each other’s genetic parts.

And they succeeded. They didn’t fade away after the sophisticated Eukaryotes began evolving into countless large species like us. Today, their total mass is right up there with all the plants and animals combined. Humans each carry around a few pounds of them.  They got the basics right. We are among the beneficiaries.

“We Are All Mutants”: Mutation Basics

In The Ancestor’s Tale: A Pilgrimage to the Dawn of Evolution (2016), Richard Dawkins writes:

The word ‘mutation’ conjures up images of grotesquely distorted creatures, perhaps generated by unscrupulous experimenters, or springing up as a consequence of some radioactive catastrophe. The truth is somewhat different. We are all mutants. The DNA passed on to us from our parents contains novel changes—mutations—which were not present in the DNA that they inherited from their parents. Fortunately so, for mutations provide the raw material, sculpted over millennia by natural selection, used to build the bodies of all the pilgrims on our journey. (126)

I’ve wanted to understand the basics of such a process that provides the “raw material” for evolution as well as a share of diseases and disabilities.  Explaining it here is a step in that direction, so here’s my version of Mutation Made Simple—very simple. I’ve omitted RNA, base pairs, and gene recombination, and I’ve compressed and approximated.

Despite simplification, though, the basics of mutations remain difficult to grasp initially for two reasons. One is that DNA duplication, even when it is on track, takes place in several steps that are difficult to visualize and it does so with four kinds of chemical players of whom three bear unfamiliar names. They are nucleotide, codon, and amino acid; the familiar fourth one is protein. Many mutations start with a miscopied nucleotide, which leads to an error in a codon, which corresponds to the wrong amino acid, which may screw up the protein. Simple.

The second difficulty is that there is “slack” in these steps. That is, many of the missteps that could lead to an actual difference in a body are corrected by the cell or produce no  result or produce a result that is harmless. A built-in “forgiveness factor” prevents every single mistake in DNA copying from invariably leading to potentially risky changes in an organism. Such a buffer in the genetic system is an important piece of its complexity.

dna and codons (

From the top: the double strand of DNA; the three-letter codons from one of the strands; and the necklace of amino acids designated by each codon. (

That said, let’s look at the normal duplication sequence. Mutations exist because cells require replacement. The first step in making a new cell is for the old one to make a copy of its DNA. DNA strands themselves consist of a line-up of basic organic molecules, the nucleotides. There are only four nucleotides, with names that are abbreviated A, C, G, and T. This is the DNA “code,” somewhat like the dots and dashes in Morse code.

The cell reads the nucleotides in groups of three. That is, the nucleotides constitute a kind of small alphabet that spells out a vocabulary of 64 three-letter “words.”  Each word or triplet, which is the codon, designates one of twenty amino acids.  (So here is one “slack” point: twenty amino acids designated by three times as many codons means each amino acid may be designated by not just one codon but by several. The result is a buffer: An incorrect codon doesn’t necessarily call up the wrong amino acid. )

Cells then build the protein molecules that will form the new cell by reading each codon, bringing the appropriate amino acid molecule into place, and stringing it like a bead on a necklace in the proper sequence. The finished molecule is the necklace of amino acids, a particular and complex protein.

But sometimes over billions of nucleotide duplications, a nucleotide miscopies; what should be a copy of an A is a T instead, a C miscopies as a G.

sickle cell (
Sickle cells among normal red blood cells. (

Take the codon TTC, for example. Let’s say that a copy of it comes out as TTA, one letter off. When this TTA later comes up in the protein production line, which amino acid does it designate and what will the impact be? Is TTA one of the few “nonsense” codons that match no amino acid all and stop the copying process before the protein is complete? Or, if it does result in a changed protein and gene, will the change be limited to one organism, or has the error occurred in a gene for sperm or the ovum that will carry it to offspring?

Point mutation (Pinterest)

The GAG codon, when it miscopies as GTG, puts into the hemoglobin protein an amino acid that creates sickle-shaped cells can bring on painful anemia but also protection against malaria. (Pinterest)

TTA, it turns out, has no such harsh consequences. The amino acid it calls up has the same function as the one that the original TTC corresponded to. The final protein functions normally. No harm, no foul—another bit of “forgiveness” in the replication process. But see the illustrations for the much less neutral mutation that produces Sickle cells in the blood.

Besides such mutations that start with the miscopying of a nucleotide, mutations can also occur in another way: through the insertion or deletion of nucleotides and codons, sometimes one codon, sometimes hundreds.

Codons are read in threes. So the insertion or deletion of even a single nucleotide changes all the codons coming after it in what’s called the frame of the gene, the full sequence of codons. To see the effect of such a seemingly minor change, delete just the first letter, t, from the following sentence of three-letter words:  “the man won the bet” becomes “hem anw ont heb et…”.  And if you inserts a single letter instead of deleting one, the chaotic effect is the same.

In other mutations, a codon or group of codons goes manic and repeats far in excess of the usual number. A gene for brain development, for example, includes from six to fifty repetitions of a CGG codon. That’s normal for that gene. But in a mutation that leads to a form of retardation called Fragile-X Syndrome, the gene repeats the CGG codon from 200 to 1000 times.

So mutations start with nucleotides and codons but may end by altering genes. Some changes are disastrous, some have little or no effect, some are passed on through generations, most are not passed on at all. But in the background, behind the grim or the helpful outcomes, mutations keep bringing forth a trickle of variations of all sorts, in all species—the modest but persistent originality of organic life itself. Untypical coloration in an insect or a flower or an animal’s fur may start out as a minor difference. But over generations, if the individuals with the coloring are a little healthier, evade a few more predators, attract more mates, or produce more offspring, the color mutation will take its place in the species.