ATP Transport Challenges the Evolutionary Origin of Mitochondria

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By Fazale Rana – August 21, 2019

In high school, I spent most Sunday mornings with my family gathered around the TV watching weekly reruns of the old Abbott and Costello movies.

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Image: Bud Abbott and Lou Costello. Image credit: Wikipedia

One of my favorite routines has the two comedians trying to help a woman get her parallel-parked car out of a tight parking spot. As Costello takes his place behind the wheel, Abbott tells him to “Go ahead and back up.” And of course, confusion and hilarity follow as Costello repeatedly tries to clarify if he is to “go ahead” or “back up,” finally yelling, “Will you please make up your mind!”

As it turns out, biologists who are trying to account for the origin of mitochondria (through an evolutionary route) are just as confused about directions as Costello. Specifically, they are trying to determine which direction ATP transport occurred in the evolutionary precursors to mitochondria (referred to as pre-mitochondria).

In an attempt to address this question, a research team from the University of Virginia (UVA) has added to the frustration, raising new challenges for evolutionary explanations for the origin of mitochondria. Their work threatens to drive the scientific community off the evolutionary route into the ditch when it comes to explaining the origin of eukaryotic cells.1

To fully appreciate the problems this work creates for the endosymbiont hypothesis, a little background is in order. (For those familiar with the evidence for the endosymbiont hypothesis, you may want to skip ahead to The Role of Mitochondria.)

The Endosymbiont Hypothesis

Most biologists believe that the endosymbiont hypothesis serves as the best explanation for the origin of complex 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.

The “poster children” of the endosymbiont hypothesis are mitochondria. Presumably, the mitochondria started its evolutionary journey 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 providing a source of ATP). In turn, the host cell provided nutrients to the endosymbiont. Presumably, 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, generating the mitonuclear genome.

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Image: Endosymbiont Hypothesis. Image credit: Wikipedia

Evidence for the Endosymbiont Hypothesis

Much of the evidence for the endosymbiotic origin of mitochondria centers around the similarity between mitochondria and bacteria. These organelles are about the same size and shape as typical bacteria and have a double membrane structure like gram-negative cells. These organelles also divide in a way that is reminiscent of bacterial cells.

Biochemical evidence also exists for the endosymbiont hypothesis. 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 also serves as evidence for the endosymbiont hypothesis. This important lipid component of bacterial inner membranes is absent in the membranes of eukaryotic cells—except for the inner membranes of mitochondria. In fact, biochemists consider cardiolipin a signature lipid for mitochondria and a vestige of the organelle’s evolutionary history.

The Role of Mitochondria

Mitochondria serve cells in a number of ways, including:

  • Calcium storage
  • Calcium signaling
  • Signaling with reactive oxygen species
  • Regulation of cellular metabolism
  • Heat production
  • Apoptosis

Arguably one of the most important functions of mitochondria relates to their role in energy conversion. This organelle generates ATP molecules by processing the breakdown products of glycolysis through the tricarboxylic acid cycle and the electron transport chain.

Biochemists refer to ATP as a high-energy compound—it serves as an energy currency for the cell, and most cellular processes are powered by ATP. One way that ATP provides energy is through its conversion to ADP and an inorganic phosphate molecule. This breakdown reaction liberates energy that can be coupled to cellular activities that require energy.

 

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Image: The ATP/ADP Reaction Cycle. Image credit: Shutterstock

ATP Production and Transport

The enzyme complex ATP synthase, located in the mitochondrial inner membrane, generates ATP from ADP and inorganic phosphate, using a proton gradient generated by the flow of electrons through the electron transport chain. As ATP synthase generates ATP, it deposits this molecule in the innermost region of the mitochondria (called the matrix or the lumen).

In order for ATP to become available to power cellular processes, it has to be transported out of the lumen and across the mitochondrial inner membrane into the cytoplasm. Unfortunately, the inner mitochondrial membrane is impermeable to ATP (and ADP). In order to overcome this barrier, a protein embedded in the inner membrane called ATP/ADP translocase performs the transport operation. Conveniently, for every molecule of ATP transported out of the lumen, a molecule of ADP is transported from the cytoplasm into the lumen. In turn, this ADP is converted into ATP by ATP synthase.

Because of the importance of this process, copies of ATP/ADP translocase comprises 10% of the proteins in the inner membrane.

If this enzyme doesn’t function properly, it will result in mitochondrial myopathies.

The Problem ATP Transport Causes for The Endosymbiont Hypothesis

Two intertwined questions confronting the endosymbiont hypothesis relate to the evolutionary driving force behind symbiogenesis and the nature of pre-mitochondria.

Traditionally, evolutionary biologists have posited that the host cell was an anaerobe, while the endosymbiont was an aerobic microbe, producing ATP from lactic acid generated by the host cell. (Lactic acid is the breakdown product of glucose in the absence of oxygen).

But, as cell biologist Franklin Harold points out, this scenario has an inherent flaw. Namely, if the endosymbiont is producing ATP necessary for its survival from host cell nutrients, why would it relinquish some—or even all—of the ATP it produces to the host cell?

According to Harold, “The trouble is that unless the invaders share their bounty with the host, they will quickly outgrow him; they would be pathogens, not symbionts.”2

And, the only way they could share their bounty with the host cell is to transport ATP from the engulfed cell’s interior to the host cell’s cytoplasm. While mitochondria accomplish this task with the ATP/ADP translocase, there is no good reason to think that the engulfed cell would do this. Given the role ATP plays as the energy currency in the cell and the energy that is expended to make this molecule, there is no advantage for the engulfed cell to pump ATP from its interior to the exterior environment.

Harold sums up the problem this way: “Such a carrier would not have been present in the free-living symbiont but must have been acquired in the course of its enslavement; it cannot be called upon to explain the initial benefits of the association.”3

In other words, currently, there is no evolutionary explanation for why the ATP/ADP translocase in the mitochondrial inner membrane—a protein central to the role of mitochondria in eukaryotic cells—pumps ATP from the lumen to the cytoplasm.

Two Alternative Models

This problem has led evolutionary biologists to propose two alternative models to account for the evolutionary driving force behind symbiogenesis: 1) the hydrogen hypothesis; and 2) the oxygen scavenger hypothesis.

The hydrogen hypothesis argues that the host cell was a methanogenic member of archaea that consumed hydrogen gas and the symbiont was a hydrogen-generating alpha proteobacteria.

The oxygen-scavenging model suggests that the engulfed cell was aerobic, and because it used oxygen, it reduced the amount of oxygen in the cytoplasm of the host cell, thought to be an anaerobe.

Today, most evolutionary biologists prefer the hydrogen hypothesis—in part because the oxygen scavenger model, too, has a fatal flaw. As Harold points out, “This [oxygen scavenger model], too, is dubious, because respiration generates free radicals that are known to be a major source of damage to cellular membranes and genes.”4

Moving Forward, Or Moving Backward?

To help make headway, two researchers from UVA attempted to reconstruct the evolutionary precursor to mitochondria, dubbed pre-mitochondria.

Operating within the evolutionary framework, these two investigators reconstructed the putative genome of pre-mitochondria using genes in the mitochondrial genome and genes from the nuclear genomes of organisms they believe were transferred to the nucleus during the process of symbiogenesis. (Genes that clustered with alphaproteobacterial genes were deemed to be of mitochondrial origin.)

Based on their reconstruction, they conclude that the original engulfed cell actually used its ATP/ADP translocase to import ATP from the host cell cytoplasm into its interior, exchanging the ATP for an ADP. This is the type of ATP/ADP translocase found in obligate intracellular parasites alive today.

According to the authors, this means that:

“Pre-mitochondrion [was] an ‘energy scavenger’ and suggests an energy parasitism between the endosymbiont and its host at the origin of the mitochondria. . . . This is in sharp contrast with the current role of mitochondria as the cell’s energy producer and contradicts the traditional endosymbiotic theory that the symbiosis was driven by the symbiont supplying the host ATP.”5

The authors speculate that at some point during symbiogenesis the ATP/ADP translocase “went ahead and backed up,” reversing direction. But, this explanation is little more than a just-so story with no evidential support. Confounding their conjecture is their discovery that the ATP/ADP translocase found in mitochondria is evolutionarily unrelated to the ATP/ADP translocases found in obligate intracellular parasites.

The fact that the engulfed cell was an obligate intracellular parasite not only brings a halt to the traditional version of the endosymbiont hypothesis, it flattens the tires of both the oxygen scavenger model and hydrogen hypothesis. According to Wang and Wu (the UVA investigators):

“Our results suggest that mitochondria most likely originated from an obligate intracellular parasite and not from a free-living bacterium. This has important implications for our understanding of the origin of mitochondria. It implies that at the beginning of the endosymbiosis, the bacterial symbiont provided no benefits whatsoever to the host. Therefore we argue that the benefits proposed by various hypotheses (e.g, oxygen scavenger and hydrogen hypotheses) are irrelevant in explaining the establishment of the initial symbiosis.”6

If the results of the analysis by the UVA researchers stand, it leaves evolutionary biologists with no clear direction when it comes to determining the evolutionary driving force behind the early stages of symbiogenesis or the evolutionary route to mitochondria.

It seems that the more evolutionary biologists probe the question of mitochondrial origins, the more confusion and uncertainty results. In fact, there is not a coherent compelling evolutionary explanation for the origin of eukaryotic cells—one of the key events in life’s history. The study by the UVA investigators (along with other studies) casts aspersions on the most prominent evolutionary explanations for the origin of eukaryotes, justifying skepticism about the grand claim of the evolutionary paradigm: namely, that the origin, design, and history of life can be explained exclusively through evolutionary processes.

In light of this uncertainty, can the origin of mitochondria, and hence eukaryotic cells, be better explained by a creation model? I think so, but for many scientists this is a road less traveled.

Resources

Challenges to the Endosymbiont Hypothesis:

In Support of a Creation Model for the Origin of Eukaryotic Cells:

ATP Production and the Case for a Creator:

Endnotes
  1. Zhang Wang and Martin Wu, “Phylogenomic Reconstruction Indicates Mitochondrial Ancestor Was an Energy Parasite,” PLOS One 9, no. 10 (October 15, 2014): e110685, doi:10.1371/journal.pone.0110685.
  2. Franklin M. Harold, In Search of Cell History: The Evolution of Life’s Building Blocks (Chicago, IL: The University of Chicago Press, 2014), 131.
  3. Harold, In Search of Cell History, 131.
  4. Harold, In Search of Cell History, 132.
  5. Wang and Wu, “Phylogenomic Reconstruction.”
  6. Wang and Wu, “Phylogenomic Reconstruction.”

Reprinted with permission by the author

Original article at:
https://www.reasons.org/explore/blogs/the-cells-design/read/the-cells-design/2018/11/21/vocal-signals-smile-on-the-case-for-human-exceptionalism

The Endosymbiont Hypothesis: Things Aren’t What They Seem to Be

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BY FAZALE RANA – AUGUST 29, 2018

Sometimes, things just aren’t what they seem to be. For example, when it comes to the world of biology:

  • Fireflies are not flies; they are beetles
  • Prairie dogs are not dogs; they are rodents
  • Horned toads are not toads; they are lizards
  • Douglas firs are not firs; they are pines
  • Silkworms are not worms; they are caterpillars
  • Peanuts are not nuts; they are legumes
  • Koala bears are not bears; they are marsupials
  • Guinea pigs are not from Guinea and they are not pigs; they are rodents from South America
  • Banana trees are not trees; they are herbs
  • Cucumbers are not vegetables; they are fruit
  • Mexican jumping beans are not beans; they are seeds with a larva inside

And . . . mitochondria are not alphaproteobacteria. In fact, evolutionary biologists don’t know what they are—at least, if recent work by researchers from Uppsala University in Sweden is to be taken seriously.1

As silly as this list may be, evolutionary biologists are not amused by this latest insight about the identity of mitochondria. Uncertainty about the evolutionary origin of mitochondria removes from the table one of the most compelling pieces of evidence for the endosymbiont hypothesis.

A cornerstone idea within the modern evolutionary framework, biology textbooks often present the endosymbiont hypothesis as a well-evidenced, well-established evolutionary explanation for the origin of complex cells (eukaryotic cells). Yet, confusion and uncertainty surround this idea, as this latest discovery attests. To put it another way: when it comes to the evolutionary explanation for the origin of complex cells in biology textbooks, things aren’t what they seem.

The Endosymbiont Hypothesis

Most evolutionary biologists believe that the endosymbiont hypothesis is the best explanation for 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 to explain the origin of eukaryotic cells in the 1960s.

Since that time, Margulis’s ideas on the origin of complex cells have become an integral part of the evolutionary paradigm. Many life scientists find the evidence for this hypothesis compelling; consequently, they 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. (Ingested cells that take up permanent residence within other cells are referred to as endosymbionts.)

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The Evolution of Eukaryotic Cells According to the Endosymbiont Hypothesis

Image source: Wikipedia

Presumably, organelles such as mitochondria were once endosymbionts. Evolutionary biologists believe that once taken inside the host cell, the endosymbionts took up permanent residence, with the endosymbiont growing and dividing inside the host. Over time, endosymbionts and hosts 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 endosymbionts’ genomes were transferred into the genome of the host organism. Eventually, the host cell evolved machinery to produce proteins needed by the former endosymbiont and processes to transport those proteins into the organelle’s interior.

Evidence for the Endosymbiont Hypothesis

The morphological similarity between organelles and bacteria serve as one line of evidence for the endosymbiont hypothesis. For example, mitochondria are about the same size and shape as a typical bacterium and they have a double membrane structure like the gram-negative cells. These organelles also divide in a way that is reminiscent of bacterial cells.

Biochemical evidence also seems to support the endosymbiont hypothesis. Evolutionary biologists view the presence of the diminutive mitochondrial genome as a vestige of this organelle’s evolutionary history. Additionally, biologists also take 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 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.

But, as compelling as these observations may be, for many evolutionary biologists phylogenetic analysis provides the most convincing evidence for the endosymbiont hypothesis. Evolutionary trees built from the DNA sequences of mitochondria, bacteria, and archaea place these organelles among a group of microbes called alphaproteobacteria. And, for many (but not all) evolutionary trees, mitochondria cluster with the bacteria, Rickettsiales.For evolutionary biologists, these results mean that the endosymbionts that eventually became the first mitochondria were alphaproteobacteria. If mitochondria were notevolutionarily derived from alphaproteobacteria, why would the DNA sequences of these organelles group with these bacteria in evolutionary trees?

But . . . Mitochondria Are Not Alphaproteobacteria

Even though evolutionary biologists seem certain about the phylogenetic positioning of mitochondria among the alphaproteobacteria, there has been an ongoing dispute as to the precise positioning of mitochondria in evolutionary trees, specifically whether or not mitochondria group with Rickettsiales. Looking to bring an end to this dispute, the Uppsula University research team developed a more comprehensive data set to build their evolutionary trees, with the hope that they could more precisely locate mitochondria among alphaproteobacteria. The researchers point out that the alphaproteobacterial genomes used to construct evolutionary trees stem from microbes found in clinical and agricultural settings, which is a small sampling of the alphaproteobacteria found in nature. Researchers knew this was a limitation, but, up to this point, this was the only DNA sequence data available to them.

To avoid the bias that arises from this limited data set, the researchers screened databases of DNA sequences collected from the Pacific and Atlantic Oceans for undiscovered alphaproteobacteria. They uncovered twelve new groups of alphaproteobacteria. In turn, they included these new genome sequences along with DNA sequences from previously known alphaproteobacterial genomes to build a new set of evolutionary trees. To their surprise, their analysis indicates that mitochondria are not alphaproteobacteria.

Instead, it looks like mitochondria belong to a side branch that separated from the evolutionary tree before alphaproteobacteria emerged. Adding to their surprise, the research team was unable to identify any bacterial species alive today that would group with mitochondria.

To put it another way: the latest study indicates that evolutionary biologists have no candidate for the evolutionary ancestor of mitochondria.

Does the Endosymbiont Hypothesis Successfully Account for the Origin of Mitochondria?

Evolutionary biologists suggest that there’s compelling evidence for the endosymbiont hypothesis. But when researchers attempt to delineate the details of this presumed evolutionary transition, such as the identity of the original endosymbiont, it becomes readily apparent that biologists lack a genuine explanation for the origin of mitochondria and, in a broader context, the origin of eukaryotic cells.

As I have written previously, the problems with the endosymbiont hypothesis are not limited to the identity of the evolutionary ancestor of mitochondria. They are far more pervasive, confounding each evolutionary step that life scientists envision to be part of the emergence of complex cells. (For more examples, see the Resources section.)

When it comes to the endosymbiont hypothesis, things are not what they seem to be. If mitochondria are not alphaproteobacteria, and if evolutionary biologists have no candidate for their evolutionary ancestor, could it be possible that they are the handiwork of the Creator?

Resources

Endnotes

  1. Joran Martijn et al., “Deep Mitochondrial Origin Outside the Sampled Alphaproteobacteria,” Nature 557 (May 3, 2018): 101–5, doi:10.1038/s41586-018-0059-5.
Reprinted with permission by the author
Original article at:
https://www.reasons.org/explore/blogs/the-cells-design/read/the-cells-design/2018/08/29/the-endosymbiont-hypothesis-things-aren-t-what-they-seem-to-be

The Multiplexed Design of Neurons

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BY FAZALE RANA – AUGUST 22, 2018

In 1910, Major General George Owen Squier developed a technique to increase the efficiency of data transmission along telephone lines that is still used today in telecommunications and computer networks. This technique, called multiplexing, allows multiple signals to be combined and transmitted along a single cable, making it possible to share a scarce resource (available phone lines, in Squier’s day).

Today, there are a number of ways to carry out multiplexing. One of them is called time-division multiplexing. While other forms of multiplexing can be used for analog data, this technique can only be applied to digital data. Data is transmitted as a collection of bits along a single channel separated by a time interval that allows the data groups to be directed to the appropriate receiver.

Researchers from Duke University have discovered that neurons employ time-division multiplexing to transmit multiple electrical signals along a single axon.1 The remarkable similarity between data transmission techniques used by neurons and telecommunication systems and computer networks is provocative. It can also be marshaled to add support to the revitalized Watchmaker argument for God’s existence and role in the origin and design of life.

A brief primer on neurons will help us better appreciate the work of the Duke research team.

Neurons

The primary component of the nervous system (the brain, spinal cord, and the peripheral system of nerves), neurons are electrically excitable cells that rely on electrochemical processes to receive and send electrical signals. By connecting to each other through specialized structures called synapses, neurons form pathways that transmit information throughout the nervous system.

Neurons consist of the soma or cell body, along with several outward extending projections called dendrites and axons.

multiplexed-design-of-neuronsImage credit: Wikipedia

Dendrites are “tree-like” projections that extend from the soma into the synaptic space. Receptors on the surface of dendrites bind neurotransmitters deposited by adjacent neurons in the synapse. These binding events trigger an electrical signal that travels along the length of the dendrites to the soma. However, axons conduct electrical impulses away from the soma toward the synapse, where this signal triggers the release of neurotransmitters into the extracellular medium, initiating electrical activity in the dendrites of adjacent neurons.

Sensory Neurons

In the world around us, many things happen at the same time. And we need to be aware of all of these events. Sensory neurons react to stimuli, communicating information about the environment to our brains. Many different types of sensory neurons exist, making possible our sense of sight, smell, taste, hearing, touch, and temperature. These sensory neurons have to be broadly tuned and may have to respond to more than one environmental stimulus at the same time. An example of this scenario would be carrying on a conversation with a friend at an outdoor café while the sounds of the city surround us.

The Duke University researchers wanted to understand the mechanism neurons employ when they transmit information about two or more environmental stimuli at the same time. To accomplish this, the scientists trained two macaques (monkeys) to look in the direction of two distinct sounds produced at two different locations in the room. After achieving this step, the researchers planted electrodes into the inferior colliculus of the monkeys’ brains and used these electrodes to record the activity of single neurons as the monkeys responded to auditory stimuli. The researchers discovered that each sound produced a unique firing rate along single neurons and that when the two sounds were presented at the same time, the neuron transmitting the electrical signals alternated back and forth between the two firing rates. In other words, the neurons employed time-division multiplexing to transmit the two signals.

Neuron Multiplexing and the Case for Creation

The capacity of neurons to multiplex signals generated by environmental stimuli exemplifies the elegance and sophistication of biological designs. And it is discoveries such as these that compel me to believe that life must stem from the work of a Creator.

But the case for a Creator extends beyond the intuition of design. Discoveries like this one breathe new life into the Watchmaker argument.

British natural theologian William Paley (1743–1805) advanced this argument by pointing out that the characteristics of a watch—with the complex interaction of its precision parts for the purpose of telling time—implied the work of an intelligent designer. Paley asserted by analogy that just as a watch requires a watchmaker, so too, does life require a Creator, since organisms display a wide range of features characterized by the precise interplay of complex parts for specific purposes.

Over the centuries, skeptics have maligned this argument by claiming that biological systems only bear a superficial similarity to human designs. That is, the analogy between human designs and biological systems is weak and, therefore, undermines the conclusion that a Divine Watchmaker exits. But, as I discuss in The Cell’s Design, the discovery of molecular motors, biochemical watches, and DNA computers—biochemical complexes with machine-like characteristics—energizes the argument. These systems are identical to the highly sophisticated machines and devices we build as human designers. In fact, these biochemical systems have been directly incorporated into nanotechnologies. And, we recognize that motors and computers, not to mention watches, come from minds. So, why wouldn’t we conclude that these biochemical systems come from a mind, as well?

Analogies between human machines and biological systems are not confined to biochemical systems. We see them at the biological level as well, as the latest work by the research team from Duke University illustrates.

It is fascinating to me that as we learn more about living systems, whether at the molecular scale, the cellular level, or the systems stage, we discover more and more instances in which biological systems bear eerie similarities to human designs. This learning strengthens the Watchmaker argument and the case for a Creator.

Resources

Endnotes

  1. Valeria C. Caruso et al., “Single Neurons May Encode Simultaneous Stimuli by Switching between Activity Patterns,” Nature Communications 9 (2018): 2715, doi:10.1038/s41467-018-05121-8.
Reprinted with permission by the author
Original article at:
https://www.reasons.org/explore/blogs/the-cells-design/read/the-cells-design/2018/08/22/the-multiplexed-design-of-neurons

Design Principles Explain Neuron Anatomy

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BY FAZALE RANA – AUGUST 15, 2018

It’s one of the classic episodes of I Love Lucy. Originally aired on September 15, 1952, the episode entitled “Job Switching” finds Lucy and Ethel working at a candy factory. They have been assigned to an assembly line, where they are supposed to pick up pieces of candy from a moving conveyor belt, wrap them, and place the candy back on the assembly line. But the conveyor belt moves too fast for Lucy and Ethel to keep up. Eventually, they both start stuffing pieces of candy into their mouths, under their hats, and in their blouses, as fast as they can as pieces of candy on the assembly line quickly move beyond their reach—a scene of comedic brilliance.

This chaotic (albeit hilarious) scene is a good analogy for how neurons would transmit electrical signals throughout the nervous system if not for the clever design of the axons that project from the nerve cell’s soma, or cell body.

The principles that undergird the design of axons were recently discovered by a team of bioengineers at the University of California, San Diego (UCSD).1 Insights such as this highlight the elegant designs that characterize biological systems—designs worthy to be called the Creator’s handiwork—no joke.

Neurons

The primary component of the nervous system (the brain, spinal cord, and the peripheral system of nerves), neurons are electrically excitable cells, thanks to electrochemical processes that take place across their cell membranes. These electrochemical activities allow the cells to receive and send electrical signals. By connecting to each other through specialized structures called synapses, neurons form pathways that transmit information throughout the nervous system. Neurologists refer to these pathways as neural circuits.

The heart of a neuron is the soma or cell body. This portion of the cell harbors the nucleus. Two sets of projections emanate from the soma: dendrites and axons. Dendrites are “tree-like” projections that extend from the soma into the synaptic space. Receptors on the surface of dendrites bind neurotransmitters deposited by adjacent neurons in the synapse. These binding events trigger an electrical signal that travels along the length of the dendrites to the soma. On the other hand, axons conduct electrical impulses away from the soma toward the synapse where this signal triggers the release of neurotransmitters into the extracellular medium, initiating electrical activity in the dendrites of adjacent neurons. Many dendrites feed the soma, but the soma gives rise to only a single axon, though the axon can branch extensively for some types of nerve cells. Axons vary significantly in terms of their diameter and length. Their diameter ranges from 1 to 20 microns. Axons can be quite long, up to a meter in length.

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Image: A Neuron. Image source: Wikipedia

The electrical excitability of neurons stems from the charge separation across its cell or plasma membrane that arises due to concentration differences in positively charged sodium, potassium, and calcium ions between the cell’s interior and exterior surroundings. This charge difference sets up a voltage across the membrane that is maintained by the activity of proteins embedded within the membranes called ion pumps. This voltage is called the resting potential. When the neuron binds neurotransmitters, this event triggers membrane-bound proteins called ion channels to open up, allowing ions to flow across the membrane. This causes a localized change in the membrane voltage that propagates along the length of the dendrite or axon. This propagating voltage change is called an action potential. When the action potential reaches the end of the axon, it triggers the release of neurotransmitters into the synaptic space.

Why Are Neurons the Way They Are?

The UCSD researchers wanted to understand the principles that undergird the neuron design, specifically why the length and diameter of the axons varies so much. Previous studies indicate that axons aren’t structured to minimize the use of cellular material—otherwise they wouldn’t be so long and convoluted. Nor are they structured for speed because axons don’t propagate electrical signals as fast as they could, theoretically speaking.

Even though the UCSD bioengineers adhere to the evolutionary paradigm, they were convinced that design principles must exist that explain the anatomy and physiology of neurons. From my perspective, their conviction is uncharacteristic of many life scientists because of the nature of evolutionary mechanisms (unguided, historically contingent processes that co-opt and cobble together existing designs to create new biological systems). Based on these mechanisms, there need not be any rationale for why things are the way they are. In fact, many evolutionary biologists view most biological systems as flawed, imperfect systems that are little more than kludge jobs.

But their conviction paid off. They discovered an elegant rationale that explains the variation in axon lengths.

Refraction Ratio

The UCSD investigators reasoned that the cellular architecture of axons may reflect a trade-off between (1) the speed of signal transduction along the axon, and (2) the time it takes the axon to reset the resting potential after the action potential propagates along the length of the axon and to ready the cell for the next round of neurotransmitter release.

To test this idea, the research team defined a quantity they dubbed the refraction ratio. This is the ratio of the refractory period of a neuron and the time it takes the electrical signal to transmit along the length of the axon. These researchers calculated the refraction ratio for 12,000 axon branches of rat basket cells. (These are a special type of neuron with heavily branched axons.) They found the information they needed for these calculations in the NeuroMorpho database. They determined that the average value for the refraction ratio was 0.92. The ideal value for the refraction ratio is 1.0. A value of 1.0 for the refraction ratio reflects optimal efficiency. In other words, the refraction ratio appears to be nearly optimal.

If not for this optimization, then signal transmission along axons would suffer the same fate as the pieces of candy on the assembly line manned by Lucy and Ethel. Things would become a jumbled mess along the length of the axons and at the synaptic terminus. And, if this happened, the information transmitted by the neurons would be lost.

The researchers concluded that the axon diameter—and, more importantly, its length—are varied to ensure that the refraction ratio remains as close to 1.0 as possible. This design principle explains why the shape, length, and width of axons varies so much. The reset time (refractory period) cannot be substantially altered. But the axon geometry can be altered, and this variation controls the transmission time of the electrical signal along the axon. To put it another way, axon geometry is analogous to slowing down or speeding up the conveyor belt to ensure that the candy factory workers can wrap as many pieces of candy as possible, without having to eat any or tuck them under their hats.

The Importance of Axon Geometry

The researchers from UCSD think that the design principles they have uncovered may be helpful in understanding some neurological disorders. They reason that if a disease leads to changes in neuronal anatomy, the axon geometry may no longer be optimized (causing the refraction ratio to deviate from its ideal value). This deviation will lead to loss of information when nerve cells transmit electrical signals through neural circuits, potentially contributing to the etiology of neurological diseases.

This research team also thinks that their insights might have use in computer technology. Understanding the importance of refraction ratio should benefit the design of machine-learning systems based on brain-like neural networks. At this time, the design of machine-learning systems doesn’t account for the time it takes for signals to reach neural network nodes. By incorporating this temporal parameter into the design, the researchers believe that they can dramatically improve the power of neural networks. In fact, this research team is now building new types of machine-learning architectures based on these new insights.2

Axon Geometry and the Case for Creation

The elegant, optimized, sophisticated, and ingenious design displayed by axon geometry is the type of evidence that convinced me, as an agnostic graduate student studying biochemistry, that life must stem from the work of a Creator. The designs we observe in biology (and biochemistry) are precisely the types of designs that we would expect to see if a Creator was responsible for life’s origin, history, and design.

On the other hand, evolutionary mechanisms (based on unguided, directionless processes that rely on co-opting and modifying existing designs to create biological innovation) are expected to yield biological designs that are inherently limited and flawed. For many life scientists, the varying length and meandering, convoluted paths taken by axons serve as a reminder that evolution produces imperfect designs, just good enough for survival, but nothing more.

And, in spite of this impoverished view of biology, the UCSD bioengineers were convinced that there must be a design principle that explained the variable length of axons. And herein lies the dilemma faced by many life scientists. The paradigm they embrace demands that they view biological systems as flawed and imperfect. Yet, biological systems appear to be designed for a purpose. And, hence, biologists can’t stop from using design language when they describe the structure and function of these systems. Nor can they keep themselves from seeking design principles when they study the architecture and operation of these systems. In other words, many life scientists operate as if life was the product of a Creator’s handiwork, though they might vehemently deny God’s influence in shaping biology—and even go as far as denying God’s existence. In this particular case, the commitment these researchers had to a de facto design paradigm paid off handsomely for them—and scientific advance.

The Converse Watchmaker Argument

Along these lines, it is provocative that the insights the researchers gleaned regarding axon geometry and the refraction ratio may well translate into improved designs for neural networks and machine-learning systems. The idea that biological designs can inspire engineering and technology advances makes possible a new argument for God’s existence—one I have named the converse Watchmaker argument.

The argument goes something like this: if biological designs are the work of a Creator, then these systems should be so well-designed that they can serve as engineering models and otherwise inspire the development of new technologies.

At some level, I find the converse Watchmaker argument more compelling than the classical Watchmaker analogy. Again, it is remarkable to me that biological designs can inspire engineering efforts.

It is even more astounding to think that engineers would turn to biological designs to inspire their work if biological systems were truly generated by an unguided, historically contingent process, as evolutionary biologists claim.

Using biological designs to guide engineering efforts seems to be fundamentally incompatible with an evolutionary explanation for life’s origin and history. To think otherwise is only possible after taking a few swigs of “Vitameatavegamin” mix.

Resources

Endnotes

  1. Francesca Puppo, Vivek George, and Gabriel A. Silva, “An Optimized Structure-Function Design Principle Underlies Efficient Signaling Dynamics in Neurons,” Scientific Reports 8 (2018): 10460, doi:10.1038/s41598-018-28527-2.
  2. Katherine Connor, “Why Are Neuron Axons Long and Spindly? Study Shows They’re Optimizing Signaling Efficiency,” UC San Diego News Center, July 11, 2018, https://ucsdnews.ucsd.edu/pressrelease/why_are_neuron_axons_long_and_spindly.
Reprinted with permission by the author
Original article at:
https://www.reasons.org/explore/blogs/the-cells-design/read/the-cells-design/2018/08/15/design-principles-explain-neuron-anatomy

Evolutionary Paradigm Lacks Explanation for Origin of Mitochondria and Eukaryotic Cells

evolutionayparadigmlacks

BY FAZALE RANA – OCTOBER 3, 2017

You carried the cross
Of my shame
Oh my shame
You know I believe it
But I still haven’t found
What I’m looking for

—Adam Clayton, Dave Evans, Larry Mullen, Paul David Hewson, Victor Reina

One of my favorite U2 songs is “I Still Haven’t Found What I’m Looking For.” For me, it’s a reminder that because of Christ, my life has meaning, purpose, and a sense of destiny. Still, I will never discover ultimate fulfillment in this world no matter how hard I search, but in the world to come—the new heaven and new earth.

Though their pursuit is scientific and not religious, many scientists have also failed to find what they have been looking for. Physicists are on a quest to find the Theory of Everything—a Grand Unified Theory (GUT) that can account for everything in physics. However, a GUT eludes them.

On the other hand, life scientists appear to have found it. They claim to have discovered biology’s GUT: the theory of evolution. Many biologists assert that evolutionary mechanisms can fully account for the origin, history, and design of life. And they are happy to sing about their discovery any chance they get.

Yet, despite this claim, the evolutionary paradigm seems to come up short time and time again when it comes to explaining key events in life’s history. And this failure serves as the basis for my skepticism regarding the evolutionary paradigm.

Currently, evolutionary biologists lack explanations for the key transitions in life’s history, including thes

  • origin of life,
  • origin of eukaryotic cells,
  • origin of sexual reproduction,
  • origin of body plans,
  • origin of consciousness,
  • and the origin of human exceptionalism.

To be certain, evolutionary biologists have proposed models to explain each of these transitions, but the models consistently fail to deliver, as a recent review article published by two prominent evolutionary biologists from the Hungarian Academy of Sciences illustrates.In this article, these researchers point out the insufficiency of the endosymbiont hypothesis—the leading evolutionary model for the origin of eukaryotic cells—to account for the origin of mitochondria and, hence, eukaryogenesis.

The Endosymbiont Hypothesis

Lynn Margulis (1938–2011) advanced the endosymbiont hypothesis for the origin of eukaryotic cells in the 1960s, building on the ideas of Russian botanist, Konstantin Mereschkowski. Taught in introductory high school and college biology courses, Margulis’s work has become a cornerstone idea of the evolutionary paradigm. This classroom exposure explains why students often ask me 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.

According to the 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.)

Presumably, organelles such as mitochondria were once endosymbionts. Once engulfed, the endosymbionts took up permanent residency within the host, with the endosymbiont 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 the machinery to produce the proteins needed by the former endosymbiont and processes to transport those proteins into the organelle’s interior.

Evidence for the Endosymbiont Hypothesis

The similarity between organelles and bacteria serve as the main line of evidence for the endosymbiont hypothesis. For example, mitochondria—which are believed to be descended from a group of alpha-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.

Biochemical evidence also exists for the endosymbiont hypothesis. 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 also serves as evidence for the endosymbiont hypothesis. 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 it a signature lipid for mitochondria and a vestige of this organelle’s evolutionary history.2

Does the Endosymbiont Hypothesis Successfully Account for the Origin of Mitochondria?

Despite the seemingly compelling evidence for the endosymbiont hypothesis, evolutionary biologists lack a genuine explanation for the origin of mitochondria, and, in a broader context, the origin of eukaryotic cells. In their recently published critical review, Zachar and Szathmary point out that evolutionary biologists have proposed over twenty different evolutionary scenarios for the mitochondrial origins that umbrella underneath the endosymbiont hypothesis. Of these, they identify eight that are reasonable, casting the others aside. Still, these eight hypotheses fail to fully account for the origin of mitochondria. The Hungarian biologists delineate twelve questions that any successful endosymbiogenesis model must answer. In turn, they demonstrate that none of these models answers all the questions. In doing so, the two researchers call for a new theory.

In the article’s abstract, the authors state, “The origin of mitochondria is a unique and hard evolutionary problem, embedded within the origin of eukaryotes. . . . Contending theories widely disagree on ancestral partners, initial conditions and unfolding events. There are many open questions but there is no comparative examination of hypotheses. We have specified twelve questions about the observable facts and hidden processes leading to the establishment of the endosymbiont that a valid hypothesis must address. There is no single theory capable of answering all questions.”3

Space doesn’t permit me to discuss each of the questions posed by the pair of biologists. Still, I would like to call attention to a few problems confronting the endosymbiont hypothesis, highlighted in their critical review.

Lack of Transitional Intermediates. Biologists have yet to discover any single-celled organisms that represent transitional intermediates between prokaryotes and eukaryotic cells. (There are some eukaryotes that lack mitochondria, but they appear to have lost these organelles.) All complex cells display the eukaryotic hallmark features. In other words, it looks as if eukaryotic cells emerged in a short period of time, without any transitional forms. In fact, some biologists dub the transition the eukaryotic big bang.

Chimeric Nature of Eukaryotic Cells. Eukaryotic cells possess an unusual combination of features. Their information-processing systems resemble those of archaea, but their membranes and energy metabolism are bacteria-like. There is no plausible evolutionary scenario to explain this blend of features. It would require the archaeon host to replace its membranes while retaining all its information-processing genes. Evolutionary biologists know of no instance in which this type of transition took place, nor do they know how it could have occurred.

Absence of Membrane Bioenergetics in the Host. All prokaryotic organisms rely on their plasma membrane to produce energy. If eukaryotic cells emerged via endosymbiogenesis, then the plasma membranes of eukaryotic cells should possess vestiges of that past function. Yet, the plasma membranes of eukaryotic cells show no traces of this essential biochemical feature.

Mechanism of Inclusion. The most plausible way for the endosymbiont to be taken up by the host cell is through a process called phagocytosis. But why wouldn’t the engulfed cell be digested by the host? How did the endosymbiont escape destruction? And, if it somehow survived, why doesn’t the mitochondria possess a triple membrane system, with the outermost membrane derived from the phagosome?

Early Selective Advantage. Once inside the host, why didn’t the endosymbiont simply reproduce, overrunning the host cell? What benefit would it be for the host cell to initially harbor the endosymbiont? Currently, evolutionary biologists don’t have answers to troubling questions such as these.

The challenges delineated by the Hungarian biologists aren’t the only ones faced by evolutionary models for endosymbiogenesis. As I discuss in a previous article, mitochondrial protein biogenesis poses another difficult problem for the endosymbiont hypothesis.

The authors of the critical review sum it up this way: “The integration of mitochondria was a major transition, and a hard one. It poses puzzles so complicated that new theories are still generated 100 years since endosymbiogenesis was first proposed by Konstantin Mereschkowsky and 50 years since Lynn Margulis cemented the endosymbiotic origin of mitochondria into evolutionary biology. . . . One would expect that by this time, there is a consensus about the transition, but far from that even the most fundamental points are still debated.”4

Though evolutionary biologists claim to have life’s history all figured out, in reality they are like most of us—they still haven’t found what they are looking for.

Resources

Endnotes

  1. Istvan Zachar and Eors Szathmary, “Breath-Giving Cooperation: Critical Review of Origin of Mitochondria Hypotheses,” Biology Direct 12 (August 14, 2017): 19, doi:10.1186/s13062-017-0190-5.
  2. In previous posts (herehere, and here), I explain the rationale for mitochondrial DNA and the presence of cardiolipin in the inner mitochondrial membrane from a creation model/intelligent design vantage point and, in doing so, demonstrate that the two biochemical features aren’t uniquely explained by the endosymbiont hypothesis.
  3. Zachar and Szathmary, “Breath-Giving Cooperation.”
  4. Zachar and Szathmary, “Breath-Giving Cooperation.”
Reprinted with permission by the author
Original article at:
https://www.reasons.org/explore/blogs/the-cells-design/read/the-cells-design/2017/10/03/evolutionary-paradigm-lacks-explanation-for-origin-of-mitochondria-and-eukaryotic-cells

Science News Flash: Has the Last Universal Common Ancestor Been Identified?

sciencenewsflashhasthelastuniversal

BY FAZALE RANA – JULY 28, 2016

Researchers from Germany made headlines by announcing that they are one step closer to identifying LUCA (the last universal common ancestor)—the single-celled organism that anchors the evolutionary tree of life.1

Because an organism’s genes reflect its environment, these researchers attempted to partially reconstruct LUCA’s genome. They reasoned that this reconstruction would tell them something about LUCA’s complexity and lifestyle.2 To accomplish this task, the researchers searched 6.1 million protein-coding genes found in archaeal and bacterial genomes for those with a special type of history (that is, they searched for universal, monophyletic genes).

They identified 355 types of genes that fit their criteria. A few of the genes appear to be involved with essential biochemical operations such as DNA replication, transcription, and translation. On the other hand, most of the 355 genes play highly specialized roles that reflect a thermophilic lifestyle. For example, they discovered an enzyme called reverse gyrase that is only found among microbes that live in high-temperature environments. They also discovered enzymes that are part of a metabolic route called the Wood-Ljungdahl pathway. This pathway uses molecular hydrogen as an electron donor, and carbon dioxide as an electron acceptor. The hydrogen had to come from a geological source. On this basis, the German scientists concluded that LUCA lived in a hydrothermal vent environment, providing a ready source for this life-giving gas.

The researchers also discovered that this microbe was able to: 1) fix nitrogen from the environment, incorporating this atom into it’s biomolecules; 2) lived in an anaerobic environment (devoid of oxygen); but 3) didn’t seem to have the ability to make amino acids. The investigators think that LUCA, though primitive, may have had more than 355 genes. If the investigators relax their search requirements a bit, they estimate that LUCA may have had nearly 575 genes.

The German research team argued that not only was LUCA a thermophile, but that the origin of life occurred at hydrothermal vents.

Have these researchers provided us with a key insight into LUCA’s identity? Have they identified the locale for the origin of life?

Not necessarily. Here are some points to consider:

In other words, there are good scientific reasons to question the high-temperature origin of life and the thermophilic identity of LUCA. And given the apparent complexity of LUCA, there is a strong basis to question evolutionary scenarios for life’s start.

In spite of the headlines, scientists have no true understanding of how chemical evolution could have produced the first life on Earth.

Resources
Too Hot to Handle” by Fazale Rana (Article)
Some Like It Hot—First Life Did Not” by Fazale Rana (Article)
Sea Vents Closed as Life-Origin Site” by Fazale Rana (Article)
Biochemists Ask, ‘How Low Can Life Go?’” by Fazale Rana (Article)
Origins of Life by Fazale Rana and Hugh Ross (Book)
Creating Life in the Lab by Fazale Rana (Book)

Endnotes

  1. Madeline C. Weiss et al., “The Physiology and Habitat of the Last Universal Common Ancestor,” Nature Microbiology 1 (July 2016): 16116, doi:10.1038/NMICROBIOL.2016.116; James O. McInerney, “Evolution: A Four Billion Year Old Metabolism,” Nature Microbiology 1 (July 2016): 16139, doi:10.1038/NMICROBIOL.2016.139.
  2. Scientists think that LUCA was a prokaryotic, single-celled microbe.
Reprinted with permission by the author
Original article at:
https://www.reasons.org/explore/blogs/the-cells-design/read/the-cells-design/2016/07/28/science-news-flash-has-the-last-universal-common-ancestor-been-identified