Mitochondria—created to energize us
by David Demick
General diagram of a mitochondrion. Mitochondria vary in size and shape, from nearly spherical to long threadlike filaments.
Mitochondria are small, membrane-bound organelles serving as energy generators in
eukaryotic cells. Most cells have hundred to thousands of them, depending on their
energy needs. Mitochondria are very good at what they do—they generate about
95% of a cell’s energy in the form of adenosine triphosphate (ATP) by oxidizing
pyruvate (a by-product of anaerobic glycolysis) to CO2 and water. They
are ovoid to filamentous in shape, generally ranging from one to seven micrometers
in length (about the same size and shape as small bacteria). Since the discovery
that mitochondria possess their own DNA, it has been frequently theorized that mitochondria
evolved from ancient bacteria ingested by larger cells. This is known as the ‘endosymbiont
theory’ of mitochondrial origin. Sometimes it is stated boldly:
‘More than a billion years ago, aerobic bacteria colonized primordial eukaryotic
cells that lacked the ability to use oxygen metabolically. A symbiotic relationship
developed and became permanent. The bacteria evolved into mitochondria, thus endowing
the host cells with aerobic metabolism, a much more efficient way to produce energy
than anaerobic glycolysis.’1
Sometimes it is stated more cautiously:
‘In the endosymbiont theory, the ancestor of the eukaryotic cell (we will
call this organism a protoeukaryote) is presumed to have been a large, anaerobic,
heterotrophic prokaryote that obtained its energy by a glycolytic pathway. Unlike
present-day bacteria, this organism had the ability to take up particulate matter
… . The endosymbiont theory postulates that a condition
arose in which a large, particularly complex, anaerobic prokaryote took up a small aerobic prokaryote into
its cytoplasm and retained it in a permanent state [emphasis added].’2
Whichever way it is stated, it is given an aura of authority and certainty by its
frequent repetition in writings on cell biology. Many students find it convincing.
However, like many evolutionary ideas, it may look solid from a distance, but gaps
appear on close scrutiny.
The evidence for the endosymbiont theory revolves around selected similarities between
mitochondria and bacteria, especially the DNA ring structure. However, these similarities
do not prove evolutionary relationship. There is no clear pathway from any one kind
of bacteria to mitochondria, although several types of bacteria share isolated points
of similarity. Indeed, the scattered nature of these similarities has left plenty
of room for a less-publicized ‘direct evolution’ theory of mitochondrial
origin, in which they never had any free-living stage.3 There is enough diversity among the mitochondria
of protozoa to make evolutionists wonder if endosymbiotic origin of mitochondria
occurred more than once.4
Mitochondrial DNA
The endosymbiont theory implies that there should be considerable autonomy for mitochondria.
This is not the case. Mitochondria are far from self-sufficient even in their DNA,
which is their most autonomous feature. Mitochondria actually have most of their
proteins coded by nuclear genes, including their DNA synthesis enzymes. For example,
human mitochondria have 83 proteins, but only 13 are coded by mtDNA (mitochondrial
DNA). Even those proteins which are coded by mtDNA often have large subunits that
are coded by nuclear DNA. These nuclear-coded mitochondrial proteins must be labelled
and transferred from the cytoplasm across two membranes. This intricate, hand-in-glove
working between mtDNA and nuclear DNA presents a major difficulty for evolutionists.
They have yet to propose a reasonable mechanism by which so many genes could be
transferred intact (along with appropriate labelling and control mechanisms) to
the nucleus.
Plants and other ‘lower creatures’ may have more mitochondrial genes
than the higher animals do, but they still fall far short of the number necessary
for free-living existence. Plants have also been found to have much more non-coding
mtDNA than the ‘higher’ animals. Referred to as ‘junk DNA’
by evolutionists, it is held to have been eliminated by evolution from the mitochondrial
genomes of the higher animals, to the point that humans have virtually no non-coding
mtDNA. Evolution seems to be remarkably unpredictable in its handling of ‘junk
DNA’, allowing it to accumulate ‘haphazardly’ in the nuclear DNA
of higher animals and man, but ‘efficiently’ eliminating it from mtDNA.
It doesn’t seem reasonable for evolutionists to have it both ways.
There are more important differences between mtDNA and nuclear or prokaryotic DNA.
The main one is that the genetic code for mtDNA differs from the standard DNA code
in slight but significant ways. Why? Evolutionists make much of the universality
of the genetic code, saying that it offers strong support for common descent of
all living things. If this is true—if the code is so highly conserved in evolution
through over a billion years and millions of species—then even a few exceptions
to the rule are hard to explain. (On the other hand, from a design standpoint the
answer may lie in the simpler protein synthetic machinery served by mtDNA, which
uses fewer tRNAs, and is less specific in codon recognition.) Lack of introns is
another important difference. The ‘higher’ mtDNA has no introns, whereas
nuclear DNA and some ‘lower’ mtDNA do have them. Again, the bacteria
from which mitochondria are supposed to have evolved also lack introns. Thus, we’re
asked to believe that the pre-mitochondrial bacteria sporadically evolved introns
as they became ‘primitive’ mitochondria, and then lost them again as
eukaryotic evolution ensued. As evolutionists grapple with the biochemical details,
the endosymbiont theory becomes more and more cumbersome and vague.5
Intracellular control
As alluded to earlier, mitochondrial numbers are controlled within each cell by
energy needs. They can also travel within cells on cytoskeletal microtubule ‘rails’
wherever energy is needed (near the ribosomes in pancreatic zymogen cells, near
the proton pumps in gastric acid-secreting cells, etc.).6 This complex intracellular control is highlighted
by a common pathological abnormality in which certain body cells become bloated
by an oversupply of mitochondria. These cells, known to medicine as ‘oncocytes’,
are packed by malformed or malfunctioning mitochondria, in which various mutations
have been detected.7,8 Also, when mutated mitochondria derived from a maternal
oocyte populate all of the body’s cells, the results can be devastating. A
whole spectrum of degenerative multisystem diseases associated with mitochondrial
mutations has been described recently, with more being discovered.9,10
Such diseases tend to affect tissues most heavily dependent on aerobic metabolism,
such as neural and muscular tissue. These observable phenomena underscore the harsh
reality that random changes in mitochondria or microbes do not produce complex new
structures and regulatory systems, but rather disease and death.
It should also be pointed out that the engulfing of bacteria by larger cells is
one of the commonest phenomena in nature, happening countless times each hour. Yet,
nothing really like the formation of mitochondria has ever been observed. There
may be rare modern examples of endosymbiosis between two different types of cells,
such as the Chlorella algae within ‘green’ paramecia. Also, infecting
or parasitic microbes can persist for a time inside of larger host cells due to
encapsulation or other protective factors. Still, these events are far from the
radical biotransformation demanded by the endosymbiont theory, and no one untainted
by evolutionary preconceptions would ever dream of classifying mitochondria as once-separate
life forms, as some evolutionists have suggested. It is essentially an ‘evolutionary
miracle’, assumed to have happened in the past, but never seen or duplicated
in the present.
Chloroplasts
Furthermore, if we accept this ‘naturalistic miracle’ of mitochondrial
origin we are forced to conclude that the same miracle happened repeatedly. Evolutionists
also postulate an endosymbiotic origin for chloroplasts, the organelles of photosynthesis
in higher plants. Chloroplasts have their own DNA, once again with a ring structure.
They are similar in some respects to present-day photosynthetic bacteria. However,
because of biochemical variety among chloroplasts (like the mitochondria), evolutionists
are once again forced toward the unlikely conclusion that their endosymbiotic origin
occurred more than once!
‘According to this endosymbiont hypothesis, eucaryotic cells started out as
anaerobic cells without mitochondria or chloroplasts and then established a stable
endosymbiotic relationship with a bacterium, whose oxidative phosphorylation system
they subverted to their own use … . Plant and algal chloroplasts seem to have
been derived later from an endocytic event involving an oxygen-evolving photosynthetic
bacterium. In order to explain the different pigments and properties found in the
chloroplasts of present-day higher plants and algae, it is usually assumed that
at least three different events of this kind occurred [emphasis added].’11
Given the enormous leaps of biochemical and genetic integration which are demanded
by the endosymbiont theory, creationist skepticism is entirely justified.
Although it is correctly admitted here that the endosymbiont scenario is actually
only a hypothesis, it is presented as the only possibility. However, as shown above,
the fine print admits that assumption and speculation are major components of this
idea.
Why do mitochondria and chloroplasts have their own DNA? Evolutionists believe that
it is a source of cellular inefficiency, and that evolution has been slowly phasing
out cytoplasmic DNA over time. (This raises the obvious question of why there is
any mtDNA left at all, to which the evolutionary response is that the process of
elimination is either incomplete or arrested.) However, viewing mtDNA as inefficient
may just be a reflection of our own ignorance of the fine details of mitochondrial
function. Deeper knowledge may show that manufacture of certain mitochondrial protein
subunits ‘on-site’ is very efficient, just as the energy-harnessing
chemistry of the mitochondrial enzymes has been shown to be.
Conclusion
Given the enormous leaps of biochemical and genetic integration which are demanded
by the endosymbiont theory, creationist skepticism is entirely justified. There
is no compelling reason to believe it unless one has already decided that evolution
is true. The creationist model, holding that structures may look similar because
they were designed to do similar jobs, is a more reasonable way to view the miracle
of mitochondria.
Related articles
Further reading
Recommended Resources
References
- DiMauro, S. and Schon, E., Mitochondrial respiratory-chain
diseases, New England Journal of Medicine 358:2656, 2003.
Return to text.
- Karp, G.,Cell Biology, 2nd edition, McGraw-Hill,
New York, p. 773, 1984. Return to text.
- Karp, ref. 2, p. 775. Return to text.
- Alberts et al., Molecular Biology of the Cell,
3rd edition, Garland Publishing Inc., New York, p. 715, 1994.
Return to text.
- Alberts et al., ref. 4, pp. 708, 709.
Return to text.
- DiMauro et al., ref. 1, p. 2665.
Return to text.
- Tallini, G., Oncocytic tumors, Virchow’s Archives
433:5, 1998. Return to text.
- Jih, D. and Morgan, M., Oncocytic metaplasia occurring in
a spectrum of melanocytic nevi, American Journal of Dermatopathology
24(6):468, December 2002. Return to text.
- DiMauroet al., ref. 1, pp. 2656–2665.
Return to text.
- Leonard, J. and Schapira, A., Mitochondrial respiratory chain
disorders I: mitochondrial DNA defects, The Lancet 355:299–304,
2000. Return to text.
- Albertset al., ref. 4, pp. 714–715.
Return to text.
| Julie I. wrote: “Thank you so much for this site! I am very blessed already. I appreciate you sharing all these helps and resources. Especially the free ones. We are grateful!” Keep the free stuff coming.  | | |
|
