Why Mitochondria Make My List of Best Biological Designs

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BY FAZALE RANA – MAY 1, 2019

A few days ago, I ran across a BuzzFeed list that catalogs 24 of the most poorly designed things in our time. Some of the items that stood out from the list for me were:

  • serial-wired Christmas lights
  • economy airplane seats
  • clamshell packaging
  • juice cartons
  • motion sensor faucets
  • jewel CD packaging
  • umbrellas

What were people thinking when they designed these things? It’s difficult to argue with BuzzFeed’s list, though I bet you might add a few things of your own to their list of poor designs.

If biologists were to make a list of poorly designed things, many would probably include…everything in biology. Most life scientists are influenced by an evolutionary perspective. Thus, they view biological systems as inherently flawed vestiges cobbled together by a set of historically contingent mechanisms.

Yet as our understanding of biological systems improves, evidence shows that many “poorly designed” systems are actually exquisitely assembled. It also becomes evident that many biological designs reflect an impeccable logic that explains why these systems are the way they are. In other words, advances in biology reveal that it makes better sense to attribute biological systems to the work of a Mind, not to unguided evolution.

Based on recent insights by biochemist and origin-of-life researcher Nick Lane, I would add mitochondria to my list of well-designed biological systems. Lane argues that complex cells and, ultimately, multicellular organisms would be impossible if it weren’t for mitochondria.1(These organelles generate most of the ATP molecules used to power the operations of eukaryotic cells.) Toward this end, Lane has demonstrated that mitochondria’s properties are just-right for making complex eukaryotic cells possible. Without mitochondria, life would be limited to prokaryotic cells (bacteria and archaea).

To put it another way, Nick Lane has shown that prokaryotic cells could never evolve the complexity needed to form cells with complexity akin to the eukaryotic cells required for multicellular organisms. The reason has to do with bioenergetic constraints placed on prokaryotic cells. According to Lane, the advent of mitochondria allowed life to break free from these constraints, paving the way for complex life.

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Figure 1: A Mitochondrion. Image credit: Shutterstock

Through Lane’s discovery, mitochondria reveal exquisite design and logical architecture and operations. Yet this is not necessarily what I (or many others) would have expected if mitochondria were the result of evolution. Rather, we’d expect biological systems to appear haphazard and purposeless, just good enough for the organism to survive and nothing more.

To understand why I (and many evolutionary biologists) would hold this view about mitochondria and eukaryotic cells (assuming that they were the product of evolutionary processes), it is necessary to review the current evolutionary explanation for their origins.

The Endosymbiont Hypothesis

Most biologists believe that the endosymbiont hypothesis is the best explanation for the origin of complex eukaryotic cells. This hypothesis states that complex cells originated when single-celled microbes formed symbiotic relationships. “Host” microbes (most likely archaea) engulfed other archaea and/or bacteria, which then existed inside the host as endosymbionts.

The presumption, then, is that organelles, including mitochondria, were once endosymbionts. Evolutionary biologists believe that, once engulfed, the endosymbionts took up permanent residency within the host cell and even grew and divided inside the host. Over time, the endosymbionts and the host became mutually interdependent. For example, the endosymbionts provided a metabolic benefit for the host cell, such as serving as a source of ATP. In turn, the host cell provided nutrients to the endosymbionts. The endosymbionts gradually evolved into organelles through a process referred to as genome reduction. This reduction resulted when genes from the endosymbionts’ genomes were transferred into the genome of the host organism.

Based on this scenario, there is no real rationale for the existence of mitochondria (and eukaryotic cells). They are the way they are because they just wound up that way.

But Nick Lane’s insights suggest otherwise.

Lane’s analysis identifies a deep-seated rationale that accounts for the features of mitochondria (and eukaryotic cells) related to their contribution to cellular bioenergetics. To understand why mitochondria and eukaryotic cells are the way they are, we first need to understand why prokaryotic cells can never evolve into large complex cells, a necessary step for the advent of complex multicellular organisms.

Bioenergetics Constraints on Prokaryotic Cells

Lane has discovered that bioenergetics constraints keep bacterial and archaeal cells trapped at their current size and complexity. Key to discovering this constraint is a metric Lane devised called Available Energy per Gene (AEG). It turns out that AEG in eukaryotic cells can be as much as 200,000 times larger than the AEG in prokaryotic cells. This extra energy allows eukaryotic cells to engage in a wide range of metabolic processes that support cellular complexity. Prokaryotic cells simply can’t afford such processes.

An average eukaryotic cell has between 20,000 to 40,000 genes; a typical bacterial cell has about 5,000 genes. Each gene encodes the information the cell’s machinery needs to make a distinct protein. And proteins are the workhorse molecules of the cell. More genes mean a more diverse suite of proteins, which means greater biochemical complexity.

So, what is so special about eukaryotic cells? Why don’t prokaryotic cells have the same AEG? Why do eukaryotic cells have an expanded repertoire of genes and prokaryotic cells don’t?

In short, the answer is: mitochondria.

On average, the volume of eukaryotic cells is about 15,000 times larger than that of prokaryotic cells. Eukaryotic cells’ larger size allows for their greater complexity. Lane estimates that for a prokaryotic cell to scale up to this volume, its radius would need to increase 25-fold and its surface area 625-fold.

Because the plasma membrane of bacteria is the site for ATP synthesis, increases in the surface area would allow the hypothetically enlarged bacteria to produce 625 times more ATP. But this increased ATP production doesn’t increase the AEG. Why is that?

The bacteria would have to produce 625 times more proteins to support the increased ATP production. Because the cell’s machinery must access the bacteria’s DNA to make these proteins, a single copy of the genome is insufficient to support all of the activity centered around the synthesis of that many proteins. In fact, Lane estimates that for bacteria to increase its ATP production 625-fold, it would require 625 copies of its genome. In other words, even though the bacteria increased in size, in effect, the AEG remains unchanged.

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Figure 2: ATP Production at the Cell Membrane Surface. Image credit: Shutterstock

Things become more complicated when factoring in cell volume. When the surface area (and concomitant ATP production) increase by a factor of 625, the volume of the cell expands 15,000 times. To satisfy the demands of a larger cell, even more copies of the genome would be required, perhaps as many as 15,000. But energy production tops off at a 625-fold increase. This mismatch means that the AEG drops by 25 percent per gene. For a genome consisting of 5,000 genes, this drop means that a bacterium the size of a eukaryotic cell would have about 125,000 times less AEG than a typical eukaryotic cell and 200,000 times less AEG when compared to eukaryotes with genome sizes approaching 40,000 genes.

Bioenergetic Freedom for Eukaryotic Cells

Thanks to mitochondria, eukaryotic cells are free from the bioenergetic constraints that ensnare prokaryotic cells. Mitochondria generate the same amount of ATP as a bacterial cell. However, their genome consists of only 13 proteins, thus the organelle’s ATP demand is low. The net effect is that the mitochondria’s AEG skyrockets. Furthermore, mitochondrial membranes come equipped with an ATP transport protein that can pump the vast excess of ATP from the organelle interior into the cytoplasm for the eukaryotic cell to use.

To summarize, mitochondria’s small genome plus its prodigious ATP output are the keys to eukaryotic cells’ large AEG.

Of course, this raises a question: Why do mitochondria have genomes at all? Well, as it turns out, mitochondria need genomes for several reasons (which I’ve detailed in previous articles).

Other features of mitochondria are also essential for ATP production. For example, cardiolipinin the organelle’s inner membrane plays a role in stabilizing and organizing specific proteinsneeded for cellular energy production.

From a creation perspective it seems that if a Creator was going to design a eukaryotic cell from scratch, he would have to create an organelle just like a mitochondrion to provide the energy needed to sustain the cell’s complexity with a high AEG. Far from being an evolutionary “kludge job,” mitochondria appear to be an elegantly designed feature of eukaryotic cells with a just-right set of properties that allow for the cellular complexity needed to sustain complex multicellular life. It is eerie to think that unguided evolutionary events just happened to traverse the just-right evolutionary path to yield such an organelle.

As a Christian, I see the rationale that undergirds the design of mitochondria as the signature of the Creator’s handiwork in biology. I also view the anthropic coincidence associated with the origin of eukaryotic cells as reason to believe that life’s history has purpose and meaning, pointing toward the advent of complex life and humanity.

So, now you know why mitochondria make my list.

Resources

Endnotes
  1. Nick Lane, “Bioenergetic Constraints on the Evolution of Complex Life,” Cold Spring Harbor Perspectives in Biology 6, no. 5 (May 2014): a015982, doi:10.1101/cshperspect.a015982.

Reprinted with permission by the author
Original article at:
https://www.reasons.org/explore/blogs/the-cells-design/read/the-cells-design/2019/05/01/why-mitochondria-make-my-list-of-best-biological-designs

Endosymbiont Hypothesis and the Ironic Case for a Creator

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BY FAZALE RANA – DECEMBER 12, 2018

i ·ro ·ny

The use of words to express something different from and often opposite to their literal meaning.
Incongruity between what might be expected and what actually occurs.

—The Free Dictionary

People often use irony in humor, rhetoric, and literature, but few would think it has a place in science. But wryly, this has become the case. Recent work in synthetic biology has created a real sense of irony among the scientific community—particularly for those who view life’s origin and design from an evolutionary framework.

Increasingly, life scientists are turning to synthetic biology to help them understand how life could have originated and evolved. But, they have achieved the opposite of what they intended. Instead of developing insights into key evolutionary transitions in life’s history, they have, ironically, demonstrated the central role intelligent agency must play in any scientific explanation for the origin, design, and history of life.

This paradoxical situation is nicely illustrated by recent work undertaken by researchers from Scripps Research (La Jolla, CA). Through genetic engineering, the scientific investigators created a non-natural version of the bacterium E. coli. This microbe is designed to take up permanent residence in yeast cells. (Cells that take up permanent residence within other cells are referred to as endosymbionts.) They hope that by studying these genetically engineered endosymbionts, they can gain a better understanding of how the first eukaryotic cells evolved. Along the way, they hope to find added support for the endosymbiont hypothesis.1

The Endosymbiont Hypothesis

Most biologists believe that the endosymbiont hypothesis (symbiogenesis) best explains one of the key transitions in life’s history; namely, the origin of complex cells from bacteria and archaea. Building on the ideas of Russian botanist Konstantin Mereschkowski, Lynn Margulis(1938–2011) advanced the endosymbiont hypothesis in the 1960s to explain the origin of eukaryotic cells.

Margulis’s work has become an integral part of the evolutionary paradigm. Many life scientists find the evidence for this idea compelling and consequently view it as providing broad support for an evolutionary explanation for the history and design of life.

According to this hypothesis, 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. Presumably, organelles such as mitochondria were once endosymbionts. Evolutionary biologists believe that once engulfed by the host cell, the endosymbionts took up permanent residency, with the endosymbiont growing and dividing inside the host.

Over time, the endosymbionts and the host became mutually interdependent. Endosymbionts provided a metabolic benefit for the host cell—such as an added source of ATP—while the host cell provided nutrients to the endosymbionts. Presumably, the endosymbionts gradually evolved into organelles through a process referred to as genome reduction. This reduction resulted when genes from the endosymbionts’ genomes were transferred into the genome of the host organism.

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Figure 1: Endosymbiont hypothesis. Image credit: Wikipedia.

Life scientists point to a number of similarities between mitochondria and alphaproteobacteria as evidence for the endosymbiont hypothesis. (For a description of the evidence, see the articles listed in the Resources section.) Nevertheless, they don’t understand how symbiogenesis actually occurred. To gain this insight, scientists from Scripps Research sought to experimentally replicate the earliest stages of mitochondrial evolution by engineering E. coli and brewer’s yeast (S. cerevisiae) to yield an endosymbiotic relationship.

Engineering Endosymbiosis

First, the research team generated a strain of E. coli that no longer has the capacity to produce the essential cofactor thiamin. They achieved this by disabling one of the genes involved in the biosynthesis of the compound. Without this metabolic capacity, this strain becomes dependent on an exogenous source of thiamin in order to survive. (Because the E. coli genome encodes for a transporter protein that can pump thiamin into the cell from the exterior environment, it can grow if an external supply of thiamin is available.) When incorporated into yeast cells, the thiamin in the yeast cytoplasm becomes the source of the exogenous thiamin, rendering E. coli dependent on the yeast cell’s metabolic processes.

Next, they transferred the gene that encodes a protein called ADP/ATP translocase into the E. coli strain. This gene was harbored on a plasmid (which is a small circular piece of DNA). Normally, the gene is found in the genome of an endosymbiotic bacterium that infects amoeba. This protein pumps ATP from the interior of the bacterial cell to the exterior environment.2

The team then exposed yeast cells (that were deficient in ATP production) to polyethylene glycol, which creates a passageway for E. coli cells to make their way into the yeast cells. In doing so, E. coli becomes established as endosymbionts within the yeast cells’ interior, with the E. coli providing ATP to the yeast cell and the yeast cell providing thiamin to the bacterial cell.

Researchers discovered that once taken up by the yeast cells, the E. coli did not persist inside the cell’s interior. They reasoned that the bacterial cells were being destroyed by the lysosomal degradation pathway. To prevent their destruction, the research team had to introduce three additional genes into the E. coli from three separate endosymbiotic bacteria. Each of these genes encodes proteins—called SNARE-like proteins—that interfere with the lysosomal destruction pathway.

Finally, to establish a mutualistic relationship between the genetically-engineered strain of E. coli and the yeast cell, the researchers used a yeast strain with defective mitochondria. This defect prevented the yeast cells from producing an adequate supply of ATP. Because of this limitation, the yeast cells grow slowly and would benefit from the E. coli endosymbionts, with the engineered capacity to transport ATP from their cellular interior to the exterior environment (the yeast cytoplasm.)

The researchers observed that the yeast cells with E. coli endosymbionts appeared to be stable for 40 rounds of cell doublings. To demonstrate the potential utility of this system to study symbiogenesis, the research team then began the process of genome reduction for the E. coli endosymbionts. They successively eliminated the capacity of the bacterial endosymbiont to make the key metabolic intermediate NAD and the amino acid serine. These triply-deficient E. coli strains survived in the yeast cells by taking up these nutrients from the yeast cytoplasm.

Evolution or Intentional Design?

The Scripps Research scientific team’s work is impressive, exemplifying science at its very best. They hope that their landmark accomplishment will lead to a better understanding of how eukaryotic cells appeared on Earth by providing the research community with a model system that allows them to probe the process of symbiogenesis. It will also allow them to test the various facets of the endosymbiont hypothesis.

In fact, I would argue that this study already has made important strides in explaining the genesis of eukaryotic cells. But ironically, instead of proffering support for an evolutionary origin of eukaryotic cells (even though the investigators operated within the confines of the evolutionary paradigm), their work points to the necessary role intelligent agency must have played in one of the most important events in life’s history.

This research was executed by some of the best minds in the world, who relied on a detailed and comprehensive understanding of biochemical and cellular systems. Such knowledge took a couple of centuries to accumulate. Furthermore, establishing mutualistic interactions between the two organisms required a significant amount of ingenuity—genius that is reflected in the experimental strategy and design of their study. And even at that point, execution of their experimental protocols necessitated the use of sophisticated laboratory techniques carried out under highly controlled, carefully orchestrated conditions. To sum it up: intelligent agency was required to establish the endosymbiotic relationship between the two microbes.

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Figure 2: Lab researcher. Image credit: Shutterstock.

Or, to put it differently, the endosymbiotic relationship between these two organisms was intelligently designed. (All this work was necessary to recapitulate only the presumed first step in the process of symbiogenesis.) This conclusion gains added support given some of the significant problems confronting the endosymbiotic hypothesis. (For more details, see the Resources section.) By analogy, it seems reasonable to conclude that eukaryotic cells, too, must reflect the handiwork of a Divine Mind—a Creator.

Resources

Endnotes

  1. Angad P. Mehta et al., “Engineering Yeast Endosymbionts as a Step toward the Evolution of Mitochondria,” Proceedings of the National Academy of Sciences, USA 115 (November 13, 2018): doi:10.1073/pnas.1813143115.
  2. ATP is a biochemical that stores energy used to power the cell’s operation. Produced by mitochondria, ATP is one of the end products of energy harvesting pathways in the cell. The ATP produced in mitochondria is pumped into the cell’s cytoplasm from within the interior of this organelle by an ADP/ATP transporter.
Reprinted with permission by the author
Original article at:
https://www.reasons.org/explore/blogs/the-cells-design/read/the-cells-design/2018/12/12/endosymbiont-hypothesis-and-the-ironic-case-for-a-creator

Mitochondria’s Deviant Genetic Code: Evolution or Creation?

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BY FAZALE RANA – APRIL 18, 2018

When I was in high school, I had the well-deserved reputation of being a wise guy—though the people who knew me then might have preferred to call me a wise—, instead. Either way, for being a wise guy, I sure didn’t display much wisdom during my teenage years.

I would like to think that I am wiser today. But, the little wisdom I do possess didn’t come easy. To quote singer and songwriter, Helen Reddy, “It’s wisdom born of pain.”

Life’s hardships sure have a way of teaching you lessons. But, I also learned that there is a shortcut to gaining wisdom—if you are wise enough to recognize it. (See what I did there?) It is better to solicit the advice of wise people than to gain wisdom through life’s bitter experiences. And, perhaps there was no wiser person ever than Solomon. Thankfully, Solomon’s wisdom was captured in the book of Proverbs. Many of life’s difficulties can be sidestepped if we are willing to heed Solomon’s advice.

Solomon gained his wisdom through observation and careful reflection. But, his wisdom also came through divine inspiration, and according to Solomon, it was through wisdom that God created the world in which we live (Proverbs 8:22–31). And, it is out of this wisdom that the Holy Spirit inspired Solomon to offer the insights found in the Proverbs.

In Psalm 104, the Psalmist (presumably David) echoes the same idea as Solomon: God created our world through wisdom. The Psalmist writes:

How many are your works, Lord!

In wisdom you made them all;

Based on Proverbs 8 and Psalm 104, I would expect God’s wisdom to be manifested in the created order. The Creator’s fingerprints—so evident in nature—should not only reflect the work of intelligent agency but also display undeniable wisdom. In my view, that wisdom should be reflected in the elegance, cleverness, and ingenuity of the designs seen throughout nature. Designs that reflect an underlying purpose. And these features are exactly what we observe when we study the biological realm—as demonstrated by recent work on aquatic mammal body size conducted by investigators from Stanford University.1

Body Sizes of Aquatic Mammals

Though the majority of the world’s mammals live in terrestrial habitats, the most massive members of this group reside in Earth’s oceans. For evolutionary biologists, common wisdom has it that the larger size of aquatic mammals reflects fewer evolutionary constraints on their body size because they live in the ocean. After all, the ocean habitat is more expansive than those found on land, and aquatic animals don’t need to support their weight because they are buoyed by the ocean.

As it turns out, common wisdom is wrong in this case. Through the use of mathematical modeling (employing body mass data from about 3,800 living species of aquatic mammals and around 3,000 fossil species), the research team from Stanford learned that living in an aquatic setting imposes tight constraints on body size, much more so than when animals live on land. In fact, they discovered (all things being equal) that the optimal body mass for aquatic mammals is around 1,000 pounds. Interestingly, the body mass distributions for members of the order Sirenia (dugongs and manatees), and the clades Cetacea (whales and dolphins), and Pinnipeds (sea lions and seals) cluster near 1,000 pounds.

Scientists have learned that the optimal body mass of aquatic mammals displays an underlying biological rationale and logic. It reflects a trade-off between two opposing demands: heat retention and caloric intake. Because the water temperatures of the oceans are below mammals’ body temperatures, heat retention becomes a real problem. Mammals with smaller bodies can’t consume enough food to compensate for heat loss to the oceans, and they don’t have the mass to retain body heat. The way around this problem is to increase their body mass. Larger bodies do a much better job at retaining heat than do smaller bodies. But, the increase in body mass can’t go unchecked. Maintaining a large body requires calories. At some point, metabolic demands outpace the capacity for aquatic mammals to feed, so body mass has to be capped (near 1,000 pounds).

The researchers noted a few exceptions to this newly discovered “rule.” Baleen whales have a body mass that is much greater than 1,000 pounds. But, as the researchers noted, these creatures employ a unique feeding mechanism that allows them to consume calories needed to support their massive body sizes. Filter feeding is a more efficient way to consume calories than hunting prey. The other exception is creatures such as otters. The researchers believe that their small size reflects a lifestyle that exploits both aquatic and terrestrial habitats.

Argument for God’s Existence from Wisdom

The discovery that the body mass of aquatic mammals has been optimized is one more example of the many elegant designs found in biological systems—designs worthy to be called the Creator’s handiwork. However, from my perspective, this optimization also reflects the Creator’s sagacity as he designed mammals for the purpose of living in the earth’s oceans.

But, instead of relying on intuition alone to make a case for a Creator, I want to present a formal argument for God’s existence based on the wisdom of biology’s designs. To make this argument, I follow after philosopher Richard Swinburne’s case for God’s existence based on beauty. Swinburne argues, “If God creates a universe, as a good workman he will create a beautiful universe. On the other hand, if the universe came into existence without being created by God, there is no reason to suppose that it would be a beautiful universe.”2 In other words, the beauty in the world around us signifies the Divine.

In like manner, if God created the universe, including the biological realm, we should expect to see wisdom permeating the designs in nature. On the other hand, if the universe came into being without God’s involvement, then there is no reason to think that the designs in nature would display a cleverness and ingenuity that affords a purpose—a sagacity, if you will. In fact, evolutionary biologists are quick to assert that most biological designs are flawed in some way. They argue that there is no purpose that undergirds biological systems. Why? Because evolutionary processes do not produce biological systems from scratch, but from preexisting systems that are co-opted through a process dubbed exaptation (by the late evolutionary biologist Stephen Jay Gould), and then modified by natural selection to produce new designs.3 According to biologist Ken Miller:

“Evolution . . . does not produce perfection. The fact that every intermediate stage in the development of an organ must confer a selective advantage means that the simplest and most elegant design for an organ cannot always be produced by evolution. In fact, the hallmark of evolution is the modification of pre-existing structures. An evolved organism, in short, should show the tell-tale signs of this modification.”4

And yet we see designs in biology that are not just optimized, but characterized by elegance, cleverness, and ingenuity—wisdom.

Truly, God is a wise guy.

Resources

Endnotes

  1. William Gearty, Craig R. McClain, and Jonathan L. Payne, “Energetic Tradeoffs Control the Size Distribution of Aquatic Mammals,” Proceedings of the National Academy of Sciences USA (March 2018): doi:10.1073/pnas.1712629115.
  2. Richard Swinburne, The Existence of God, 2nd ed. (New York: Oxford University Press, 2004), 190–91.
  3. Stephen Jay Gould and Elizabeth S. Vrba, “Exaptation: A Missing Term in the Science of Form,” Paleobiology8 (January 1, 1982): 4–15, doi:10.1017/S0094837300004310.
  4. Kenneth R. Miller, “Life’s Grand Design,” Technology Review 97 (February/March 1994): 24–32.
Reprinted with permission by the author
Original article at:
https://www.reasons.org/explore/blogs/the-cells-design/read/the-cells-design/2018/04/11/mitochondria-s-deviant-genetic-code-evolution-or-creation

Can a Creation Model Explain the Origin of Mitochondria?

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BY FAZALE RANA – NOVEMBER 23, 2016

Some called her a scientific heretic. Others were a bit more kind, describing her as a maverick.

Lynn Margulis (1938–2011) earned her reputation in the late 1960s when she proposed the endosymbiont hypothesis for the origin of eukaryotic cells. Because her ideas about evolution didn’t conform to Darwinian principles, evolutionary biologists summarily dismissed her idea out of hand and then went on to ignore her work for a couple of decades. She was ultimately vindicated, however, as the endosymbiont hypothesis gradually gained acceptance.

Today, Margulis’s proposal has become a cornerstone idea of the evolutionary paradigm and is taught in introductory high school and college biology courses. This classroom exposure explains why I am often asked about the endosymbiont hypothesis when I speak on university campuses. Many first-year biology students and professional life scientists alike find the evidence for this idea compelling, and consequently view it as providing broad support for an evolutionary explanation for the history and design of life.

Yet, new work by biochemists from Cambridge University make it possible to account for the origin of eukaryotic cells from a creation model perspective, providing a response to the endosymbiont hypothesis.1

The Endosymbiont Hypothesis

According to this hypothesis, 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. (Ingested cells that take up permanent residence within other cells are referred to as endosymbionts.)

Accordingly, organelles, such as mitochondria, were once endosymbionts. Once taken inside the host cell, the endosymbionts presumably took up permanent residency within the host, with the endosymbionts growing and dividing inside the host. Over time, the endosymbionts and the host became mutually interdependent, with the endosymbionts providing a metabolic benefit for the host cell. The endosymbionts gradually evolved into organelles through a process referred to as genome reduction. This reduction resulted when genes from the endosymbionts’ genomes were transferred into the genome of the host organism. Eventually, the host cell evolved both the machinery to produce the proteins needed by the former endosymbiont and the processes needed to transport those proteins into the organelle’s interior.

Evidence for the Endosymbiont Hypothesis

The main line of evidence for the endosymbiont hypothesis is the similarity between organelles and bacteria. For example, mitochondria—which are believed to be descended from a group of α-proteobacteria—are about the same size and shape as a typical bacterium and have a double membrane structure like gram-negative cells. These organelles also divide in a way that is reminiscent of bacterial cells.

There is also biochemical evidence for the endosymbiont hypothesis. Evolutionary biologists view the existence of the diminutive mitochondrial genome as a vestige of this organelle’s evolutionary history. Additionally, the biochemical similarities between mitochondrial and bacterial genomes are taken as further evidence for the evolutionary origin of these organelles.

The presence of the unique lipid called cardiolipin in the mitochondrial inner membrane also serves as evidence for the endosymbiont hypothesis. Cardiolipin is an important lipid component of bacterial inner membranes, yet it is not found in the membranes of eukaryotic cells—except for the inner membranes of mitochondria. In fact, biochemists consider it a signature lipid for mitochondria and a vestige of this organelle’s evolutionary history.

A Creation Model Perspective on Mitochondria

So, as a creationist, how do I make sense of the evidence for the endosymbiont hypothesis?

Instead of focusing my efforts on refuting the endosymbiont hypothesis, here, I take a different approach. I maintain that it is reasonable to view eukaryotic cells as the work of a Creator, with the shared similarities between mitochondria and bacteria reflecting common design rather than common descent.

However, to legitimately interpret mitochondrial origins from a creation model perspective, there must be a reason for the biochemical similarities between mitochondria and bacteria. Previously, I wrote about discoveries that provide a rationale for why mitochondria have their own genomes. (See “Resources.”) Thanks to recent research advances, an explanation now exists for why the mitochondrial inner membranes harbor cardiolipin.

Cardiolipin’s Function

Previous studies identified close associations between cardiolipin and a number of proteins found in the mitochondrial inner membrane. These proteins play a role in harvesting energy for the cell to use. Compared to other lipid components found in the inner membrane, cardiolipin appears to preferentially associate with these proteins. Evidence indicates that cardiolipin helps to stabilize the structures of these proteins and serves to organize the proteins into larger functional complexes within the membrane.2 In fact, several studies have implicated defects in cardiolipin metabolism in the onset of a number of neuromuscular disorders.

The work of the Cambridge University investigators adds to this insight. These researchers were using computer simulations to model the interactions between cardiolipin and a protein complex called F1-F0 ATPase. Embedded within the inner membrane of mitochondria, this complex is a biomolecular rotary motor that produces the compound ATP—an energy storage material the cell’s machinery uses to power its operations.

Like other proteins found in the inner membrane, cardiolipin forms a close association with F1-F0 ATPase. However, instead of permanently binding to the surface of the protein complex, cardiolipin dynamically interacts with this membrane-embedded protein complex. The researchers think that this dynamic association and the unusual chemical structure of cardiolipin (which gives it the flexibility to interact with a protein surface) are critical for its role within the mitochondrial inner membrane. As it turns out, cardiolipin not only stabilizes the F1-F0 ATPase complex (as it does for other inner membrane proteins), but it also lubricates the protein’s rotor, allowing it to turn in the viscous cell membrane environment. Also, its unique structure helps move protons through the F1-F0 ATPase motor, providing the electrical power to operate this biochemical motor.

The bottom line: There is an exquisite biochemical rationale for why cardiolipin is found in mitochondrial inner membranes (and bacterial membranes). In light of this new insight, it is reasonable to view the shared similarities between these organelles and bacteria as reflecting common design—the product of the Creator’s handiwork. Like most biological systems, this organelle appears to be designed for a purpose.

Resources
Why Do Mitochondria Have DNA?” by Fazale Rana (article)
Mitochondrial Genomes: Evidence for Evolution or Creation?” by Fazale Rana (article)
Complex Protein Biogenesis Hints at Intelligent Design” by Fazale Rana (article)
Archetype or Ancestor? Sir Richard Owen and the Case for Design” by Fazale Rana (article)
Nanodevices Make Megascopic Statement” by Fazale Rana (article)

Endnotes

  1. Anna Duncan, Alan Robinson, and John Walker, “Cardiolipin Binds Selectively but Transiently to Conserved Lysine Residues in the Rotor of Metazoan ATP Synthases,” Proceedings of the National Academy of Sciences USA 113 (August 2016): 8687–92, doi:10.1073/pnas.1608396113.
  2. Giuseppe Paradies et al., “Functional Role of Cardiolipin in Mitochondrial Bioenergetics,” Biochimica et Biophysica Acta—Bioenergetics 1837 (April 2014): 408–17, doi:10.1016/j.bbabio.2013.10.006.
Reprinted with permission by the author
Original article at:
https://www.reasons.org/explore/blogs/the-cells-design/read/the-cells-design/2016/11/23/can-a-creation-model-explain-the-origin-of-mitochondria