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

theendosymbionthypothesis

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.)

the-endosymbiont-hypothesis

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

multiplexeddesignneurons

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

designprinciples

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.

design-principles-explain-neuron-anatomy

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

Evolution’s Flawed Approach to Science

evolutionsflawedapproach

BY FAZALE RANA – AUGUST 8, 2018

One of the things I find most troubling about the evolutionary paradigm is the view it fosters about the nature of biological systems—including human beings.

Evolution’s mechanisms, it is said, generate biological innovations by co-opting existing designs and cobbling them together to create new ones. As a result, many people in the scientific community regard biological systems as fundamentally flawed.

As biologist Ken Miller explains in an article for Technology Review:

“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.1″

So, instead of regarding humans as “fearfully and wonderfully made” (as Scripture teaches), the evolutionary paradigm denigrates human beings, as a logical entailment of its mechanisms. It renders human beings as nothing more than creatures that have been cobbled together by evolutionary mechanisms.

Adding to this concern is the impact that the evolutionary paradigm has on scientific advance. Because many in the scientific community view biological systems as fundamentally flawed, they are predisposed to conclude—oftentimes, prematurely—that biological systems lack function or purpose when initial investigations into these systems fail to uncover any obvious rationale for why these systems are the way they are. And, once these investigators conclude that a biological system is flawed, the motivation to continue studying the system dissipates. Why try to understand a flawed design? Why focus attention on biological systems that lack function? Why invest research dollars studying systems that serve no purpose?

I would contend that viewing biological systems as the Creator’s handiwork provides a superior framework for promoting scientific advance, particularly when the rationale for the structure and function of a particular biological system is not apparent. If biological systems have been created, then there must be good reasons why these systems are structured and function the way they do. And this expectation drives further study of seemingly nonfunctional, purposeless systems with the full anticipation that their functional roles will eventually be uncovered.

Recent history validates the creation model approach. During the course of the last couple of decades, the scientific community has made discovery after discovery demonstrating (1) function for biological systems long thought to be useless evolutionary vestiges, or (2) an ingenious rationale for the architecture and operation of systems long regarded as flawed designs. (For examples, see the articles listed in the Resources section.)

These discoveries were made not because of the evolutionary paradigm but in spite of it.

So often, creationists and intelligent design proponents are accused of standing in the way of scientific advance. Skeptics of creation claim that if we conclude that God created biological systems, then science grinds to a halt. If God made it, then why continue to investigate the system in question?

But, I would assert that the opposite is true. The evolutionary paradigm stultifies science by viewing biological systems as flawed and vestigial. Yet, for the biological systems discussed in the articles listed in the Resources section, the view spawned by the evolutionary paradigm delayed important advances that could have been leveraged for biomedical purposes sooner, alleviating a lot of pain and suffering.

Because a creation model perspective regards designs in nature as part of God’s handiwork, it provides the motivation to keep pressing forward, seeking a rationale for systems that seemingly lack purpose. In the handful of instances in which the scientific community has adopted this mindset, it has been rewarded, paving the way for new scientific insight that leads to biomedical breakthroughs.

Resources

Endnotes

  1. 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/2018/08/08/evolution-s-flawed-approach-to-science

“Silenced” B Cells Loudly Proclaim the Case for a Creator

silencedbcells

BY FAZALE RANA – AUGUST 1, 2018

When I was an undergraduate student studying chemistry and biology, I hated the course work I did in immunology. The immune system is fascinating, to be certain. And, as a student, I marveled at how our body defends itself from invading microorganisms. But, I hated trying to keep track of the bewildering number of the cells that comprise the immune system.

But my efforts to learn about these cells has finally paid off. It allows me to appreciate the recently discovered insights into the role “silenced” B cells play in the immune system. Not only do these insights have important biomedical implications, but, in my view, they also add to the mounting evidence for creation and further validate a creation model approach to biology.

First discovered thirty years ago, these cells were initially deemed nonfunctional junk produced by a flawed immune system. And this view has persisted for three decades.Immunologists viewed silenced B cells as harmful. Presumably, these cells impair immune system function by cluttering up immune tissues. Or worse, they considered these cells to be potentially deadly, contributing to autoimmune disorders. Yet, immunologists are changing their view of’silenced B cells, thanks to the efforts of researchers from Australia.1

A Brief (and Incomplete) Primer on Immunology

To understand the newly discovered role silenced B cells play in the immune system, a brief primer on immunology is in order.

It goes without saying that the immune system’s job is to protect the body from pathogens. To do this, it must recognize pathogens as foreign materials. To put it another way, it must distinguish self from nonself. (Autoimmune disorders result when the immune system mistakes the body’s own tissues as foreign materials, and then attacks itself.)

An incredibly complex biological system, the immune system contains one component called the humoral immune system. This part of the immune system relies on proteins, such as antibodies, circulating in extracellular fluids to mediate the body’s immune response.

Plasma cells secrete antibodies into the circulatory system. Antibodies then bind to the invading pathogen, decorating its surface. The antibodies serve as a beacon that attracts certain immune cells, such as macrophages and killer cells, that will engulf the pathogen, clearing it from the body.

Plasma cells originate in bone marrow as B cells (also known as B lymphocytes). B cells develop from hematopoietic stem cells. As they develop, genes in the developing B cell genome that encode for antibodies (and receptor proteins) undergo rearrangements (just like shuffling a deck of cards). These rearrangements generate genes that encode an ensemble of receptor proteins that reside on the B cell surface, with each receptor protein (and corresponding antibody) recognizing and binding a specific pathogen. Collectively, these cell surface receptors (and antibodies) can detect a large and varied number of foreign agents.

silenced-b-cells-loudly-proclaim-case-for-creator

Image credit: Shutterstock

After developing in the bone marrow, B cells migrate to either the spleen or lymph nodes. Here, the B cells are exposed to the flow of lymph, the fluid that moves through the lymphatic circulatory system. If pathogens have invaded the body, they will encounter B cells in lymph tissue. If a B cell has a receptor that recognizes that particular pathogen, it will bind it. This binding event will trigger the transformation of the B cell. Once activated by the binding event, the B cell migrates into a region of the lymph tissue called the germinal center. Here the B cells undergo clonal expansion, rapidly proliferating into plasma cells and memory B cells. The plasma cells produce antibodies that help identify the pathogen as a foreign invader. The memory B cells hang around in the immune tissue so the immune system can rapidly respond to that pathogen if it invades the body in the future.

A Flaw in the Immune System?

During the B cell maturation process in the bone marrow, about 50 percent of the nascent B cells produce cell surface receptors that bind to materials in the body, instead of pathogens. That is, these B cells can’t discriminate self from nonself. This outcome is a by-product of the random-shuffling mechanism that generates protein receptor diversity. The random shuffling of the genes is equally likely to produce receptors that bind to materials in the body as it is pathogens. But when this misidentification happens, an elaborate quality control system kicks in, either eliminating the faulty B cells or reworking them so that they can be a functioning part of the immune system. This reworking process involves additional gene shuffling with the hope of generating cell receptors that recognize foreign materials.

However, a few of the faulty B cells escape destruction and avoid having their genes reshuffled. In this case, the immune system silences these cells (called anergic cells), but they still hang around in immune tissue, clogging things up. It seemingly gets worse: if these cells become activated they can cause an autoimmune reaction—just the type of sloppy design evolutionary mechanisms would produce. Or is it?

A Critical Role for Silenced B Cells

Recent work by the research team from Australia provides a rationale for the persistence of silenced anergic B cells in the immune system. These cells play a role in combating pathogens such as HIV and campylobacter, which cloak themselves from the immune system by masquerading as part of our body. While these pathogens escape detection by most of the components of our immune system, they can be detected by silenced B cells with receptors that recognize self as nonself.

The silenced B cells are redeemed by the immune system in the germinal center through a process called receptor revision. Here the genes that encode the receptors experience hypermutation, altering their receptors to the extent that they now can recognize foreign materials. But the capacity of the receptors to recognize self serves the immune system well when infectious agents such as HIV or campylobacter invade.

The researchers who made the discovery think that this insight might one day help pathologists do a better job treating autoimmune disorders. They also hope it might lead to a vaccine for HIV.

A Remarkable Turnaround

In a piece for Science Alert, journalist Peter Dockrill summarizes the significance of the discovery: “It’s a remarkable turnaround for a class of immune cells long mistaken for dangerous junk—and one which shows there’s still so much we have to learn about what the immune system can do for us, and how its less than perfectly obvious mechanisms might be leveraged to do us good.”2

The surprise expressed by Dockrill reflects the influence of the evolutionary paradigm and the view that biological systems must be imperfect because of the nature of evolutionary mechanisms. And yet this discovery (along with others discussed in the articles listed in the Resources section) raises questions for me about the validity of the evolutionary paradigm. And it raises questions about the usefulness of this paradigm, as well. Viewing silenced B cell as the flawed outcome of evolutionary processes has stood in the way of discovering their functional importance, delaying work that “might be leveraged to do us good.”

The more we learn about biological systems, the more evident it becomes: Instead of being flawed, biological designs display an ingenuity and a deep rationale for the way they are—as would be expected if they were the handiwork of a Creator.

Resources

Endnotes

  1. Deborah L. Burnett et al., “Germinal Center Antibody Maturation Trajectories Are Determined by Rapid Self/Foreign Discrimination,” Science 360 (April 13, 2018): 223–26, doi: 10.1126/science.aa03859; Ervin E. Kara and Michel C.Nussenzweig, “Redemption for Self-Reactive Antibodies,” Science 360 (April 13, 2018): 152–53, doi:10.1126/science.aat5758.
  2. Peter Dockrill, “Immune Cells We Thought Were ‘Useless’ Are Actually a Weapon Against Infections Like HIV,” Science Alert (April 16, 2018), https://www.sciencealert.com/new-discovery-bad-immune-cells-actually-secret-weapon-against-infection-b-silenced-redemption-lymphocytes.
Reprinted with permission by the author
Original article at:
https://www.reasons.org/explore/blogs/the-cells-design/read/the-cells-design/2018/08/01/silenced-b-cells-loudly-proclaim-the-case-for-a-creator