What are the key events in your life’s history? What happenings shaped the person you have become? Perhaps they include events such as:
Your birth
The first day of school
The day you graduated from high school, college, or graduate school
Your first job
The day you got engaged
The day you got married
The days your children were born
The day you retired
There are also key events in the history of life on Earth. These events shaped Earth’s biosphere and explain why life looks the way it does today.
One of those key events was the emergence of eukaryotic (or complex) cells. Fossil evidence for eukaryotic cells appears in the geological column around 2 billion years ago, and chemical markers recovered from the geological column suggest eukaryotes may have been present on Earth as early as 2.8 billion years ago. The appearance of eukaryotic cells paved the way for the emergence of complex multicellular organisms such as fungi, plants, and animals.
Explaining the origin of eukaryotic cells is one of the key research problems confronting life scientists. For this reason, this problem attracts a lot of interest. As a case in point, a researcher from the University of Oxford in the UK recently discovered an important clue that has bearing on the origin of eukaryotic cells. His work explains why organelles such as mitochondria have genomes that encode a small number of proteins, with most of the organelle’s genes located in the nuclear genome.1
On the surface, this discovery seemingly provides support for the leading evolutionary explanation for the origin of eukaryotic cells—the endosymbiont hypothesis. But, upon careful reflection, it becomes clear that this work can also be marshaled to support a radically different model for the origin of eukaryotes—one that evokes a Creator’s intervention to explain the genesis of Eukarya.
The Endosymbiont Hypothesis The endosymbiont hypothesis is the leading evolutionary model for the origin of eukaryotic cells. (Readers who are familiar with endosymbiogenesis should feel free to skip ahead to Scientific Challenges for Endosymbiogenesis.)
Russian botanist Konstantin Mereschkowsky initially proposed this model in the early 1900s and biologist Lynn Margulis advanced it in the late 1960s. Today, endosymbiont theory is widely assumed to be the explanation for the origin of eukaryotic cells. According to this idea, complex cells originated when symbiotic relationships formed among single-celled microbes after free-living bacterial and/or archaeal cells were engulfed by a “host” microbe.
Much of the work on the endosymbiont hypothesis centers around the origin of the mitochondrion. In some respects, the focus on the evolutionary origin of this organelle has become emblematic of the endosymbiont hypothesis. Presumably, the organelle started as an endosymbiont. Evolutionary biologists believe that once engulfed by the host cell, this microbe took up permanent residency, growing and dividing inside the host. Over time, the endosymbiont and the host became mutually interdependent, with the endosymbiont providing a metabolic benefit for the host cell such as supplying a source of ATP. In turn, the host cell provided nutrients to the endosymbiont. Over time, the endosymbiont gradually evolved into an organelle through a process referred to as genome reduction. This reduction resulted when genes from the endosymbiont’s genome were transferred into the genome of the host organism.
Evidence for the Endosymbiont Hypothesis For evolutionary biologists, at least three lines of evidence bolster the endosymbiont hypothesis:
The similarity of mitochondria to bacteria. Most of the evidence for the endosymbiont hypothesis centers around the fact that mitochondria are about the same size and shape as a typical bacterium and have a double membrane structure like gram-negative bacteria. These organelles also divide in a way that is reminiscent of bacterial cells.
Mitochondrial DNA. Evolutionary biologists view the presence of the diminutive mitochondrial genome as a vestige of this organelle’s evolutionary history. They see the biochemical similarities between mitochondrial and bacterial genomes as further evidence for the evolutionary origin of these organelles.
The presence of the unique lipid cardiolipin in the mitochondrial inner membrane. This important lipid component of bacterial inner membranes is not found in the membranes of eukaryotic cells—except for the inner membranes of mitochondria. In fact, biochemists consider cardiolipin a signature lipid for mitochondria and another relic from its evolutionary past.
Scientific Challenges for Endosymbiogenesis Despite the impressive collection of evidence for endosymbiogenesis, this theory still faces some significant—perhaps even intractable—hurdles that include:
Accounting for the origin of protein transport into the mitochondria
Accounting for the origin of the ATP transporter in mitochondrial membranes
Accounting for the lipid divide in the eukaryotic cell membranes
(I have detailed some of these problems. See the articles listed under Resources for Further Exploration.)
These challenges do not necessarily invalidate endosymbiogenesis as the explanation for the origin of eukaryotic cells. Some advocates of the evolutionary paradigm would argue that these issues highlight the reality that the origin of eukaryotic cells is a hard problem that may well be an impenetrable scientific mystery. Fair enough. But, in light of these difficulties, no one can justifiably claim that a well-established evolutionary explanation for the origin of eukaryotic cells exists. It doesn’t.
On the other hand, these problems hold enough significance to fuel my skepticism about the all-sufficiency of evolutionary mechanisms to fully account for the origin, design, and history of life. They also point the way to alternative explanations for the genesis of eukaryotic cells that evoke the work of a Mind.
A Creation Model for the Origin of Eukaryotic Cells While many life scientists view the shared features between bacteria and mitochondria as evidence for the evolutionary origin of this organelle, it is possible to advance a different interpretation of their shared features. In a creation model, the homologies between bacteria and mitochondria are understood as shared design features.
The Why Questions For a creation model to have credibility, it must answer some important why questions, such as:
Why do organelles such as mitochondria have genomes?
Why are these genomes so diminutive with respect to the number of genes they harbor?
Why are most organellar genes stored in the nuclear genome?
If a creation model can’t offer a rationale for these features of mitochondria and other organelles such as chloroplasts, then the homologous features in bacteria and mitochondria would be best explained as evidence for common descent.
Yet, a rationale does exist. There are sound reasons for why organelles have diminutive genomes with most of their genes stored in the nucleus. (See the Resources for Further Exploration section.) And now, recent insights from Steven Kelly at the University of Oxford can be added to these reasons.
Cellular Economics of Mitochondrial Genomes Organelles like mitochondria require well over 1,000 different types of proteins to carry out their operations. But their genomes encode fewer than 100. The bulk of these proteins are encoded by genes harbored in the DNA located within the cell nucleus.
These organellar proteins are produced at ribosomes located in the cytosol. Once manufactured, the proteins must be targeted to the organelle (in this case, the mitochondria) and then imported into the organelle. Once imported, the proteins must then be sorted so that they arrive at the right location (the matrix, the inner membrane, the intermembrane space, or the outer membrane) within the mitochondria. This process requires energy and cellular resources.
Yet, Kelly learned that less energy and resources are expended by this set of processes than if organelles had genomes that encoded their full set of proteins.
This unexpected discovery makes sense in light of the number of organelles found in the cell. For example, cells harbor tens of thousands of mitochondria. Before cells divide, they must duplicate their mitochondria so that the resulting daughter cells will have enough of these organelles to sustain their energy demands. (One of the functions of mitochondria is to produce energy for the cell. For this reason, mitochondria are nicknamed the cell’s powerhouses.) Before mitochondria divide, their DNA must be replicated. DNA replication is also an energy and resource-intensive process.
Here is how it all cashes out. For the sake of discussion, let’s say that there are 50,000 mitochondria in a cell. If each mitochondrion had a full genome, then each mitochondrial gene would have to be replicated 50,000 times before cell division occurred. If, however, these genes were stored in the cell’s nucleus, then they would only have to be replicated a single time in preparation for cell division. This large discrepancy more than compensates for the energy requirements to target, import, and sort organelles’ proteins.
Proteins that are needed in high abundance in the organelles constitute an exception to the energy savings. In these cases, the energy savings that comes from locating their genes in the nucleus becomes offset by the cost of importing them into organelles. As it turns out, the proteins that are encoded in mitochondrial genomes (and the genomes of chloroplasts) are high-abundance proteins.
Other Reasons for Encoding Proteins in Mitochondrial Genomes Previous studies also indicated that the proteins encoded by mitochondrial genomes are rich in hydrophobic amino acids. This feature makes it nearly impossible for the cell’s machinery to target these proteins to mitochondria. Instead, the proteins often become “mistargeted” to the endoplasmic reticulum. The only way to ensure that the proteins make their way to the appropriate location in the mitochondria is to encode them in the mitochondrial genome and produce these proteins within the lumen of the mitochondria.
Researchers have also learned that the proteins encoded in mitochondrial genomes are the very ones that form the electron transport chain. (This biochemical system plays a central role in energy production.) By encoding these proteins in mitochondrial genomes, the cell is afforded greater regulatory control over mitochondria, making it more versatile in response to changes in its energy status. In other words, a confluence of factors—that all reinforce one another—accounts for the presence and diminutive size of organellar genomes and the presence of organellar genes in the nuclear genome.
The Best Explanation? Working from within the evolutionary paradigm, Kelly interprets his findings as uncovering the “evolutionary driving force” needed to relocate genes from endosymbiont genomes to the nuclear genome during the process of endosymbiogenesis.
Yet, having an evolutionary driving force isn’t enough. There must be a sound explanation for how the protein transport system evolved for mitochondria and chloroplasts. As I have previously argued, the integrated complexity of the protein transport system makes it hard to think that protein transport and sorting could have evolved through unguided, historically contingent processes.
It is also remarkable to think—from an evolutionary vantage point—that the selective pressures that shaped the mitochondrial genomes all align. These include (1) the high GC content of the genes, (2) the high abundance of hydrophobic amino acids that make up the proteins, (3) the metabolic role of the proteins, and (4) the organellar abundance of the proteins.
How fortuitous!
In my view as a biochemist, the serious (maybe even intractable) scientific problems confronting the endosymbiont hypothesis and the elegant rationale for mitochondrial features make best sense from a creation model standpoint.
Could it be that a Creator shaped life’s history on Earth? The evidence increasingly points in that direction.
