Wednesday, April 25, 2012

Mighty Mitochondria and the Endosymbiosis Theory


         Scientists approximate that bacteria first appeared on Earth around 3.5 billion years ago, while the first eukaryotes were not thought to inhabit Earth until approximately 1.5 billion years ago. What happened in this time gap of 2 billion years? Well, scientists can only make an educational guess, considering that primates likely did not come to be until approximately 65 million years ago (1). The endosymbiosis theory points to perhaps the earliest known form of mutualism in which bacteria are thought to have inhabited a “primordial eukaryotic cell” (2). The presence of a bacterial organism inside the larger cell allowed cellular life to adapt to the harsh conditions of the time. Scientists believe that photosynthetic bacteria appeared 3.2 million years ago, thereby releasing oxygen into the atmosphere. Oxygen can actually be a toxic substance, but the first aerobic bacteria lived about 2.5 billion years ago, very shortly before the first aerobic eukaryotes. These inferences, among many other observations, point to the endosymbiosis theory as a plausible explanation for adaption to an environment abundant in oxygen (1).

                                                                      Endosymbiosis Theory: 

Cost/Benefit Analysis          

          Why would we think that bacteria would crawl inside of another cell? Well, we assume that in a mutualistic relationship, both parties benefit due to the relationship. Additionally, the endosymbiosis theory suggests that mitochondria and chloroplasts’ lineages can be traced back to ancient bacteria. Not only are these structures about the size of a bacterium (70S), but these organelles also contain their own DNA in the form of one circular chromosome like bacteria (3). Both bacteria and the organelles replicate via binary fission (1).
Rickettsia prowazekki

         Although this background information is necessary in understanding the basic evolution of the eukaryotic cell, I would like to specifically examine the relationship between mitochondria (derived from ancient bacteria) and the primitive eukaryotic cell. As previously stated, at the time of the initial endosymbiotic encounter, few species were equipped to convert oxygen into another substance to avoid oxidation. Therefore, the host cell greatly benefitted from its smaller counterpart because mitochondria convert oxygen to ATP via substrate-level phosphorylation. Today, researchers have evidence to suggest the mitochondria are related to the proteobacterium Rickettsia prowazekii, “an obligate intracellular parasite” (3) due to its similarity in genomic sequence. Although it is not exactly clear why the bacterium benefitted from the relationship, it can be inferred that the bacterium was provided a “safe” environment to reside in a chemically stable environment. This idea applies to chloroplasts as well.

Mitochondria and the Cell
         To understand the role of early bacteria in the cell, let us look at the function of a mitochondrion. Ultimately converting oxygen to ATP, mitochondria are the powerhouses of a cell through their production of energy. Mitochondria have two membranes, of which the outer membrane, containing porins, resembles Gram-negative bacteria. The inner membrane contains cristae, infoldings that greatly increase surface area. The inside of the mitochondria, the mitochondrial matrix, contains ribosomes (similar to size of those of bacteria), DNA, and calcium phosphate granules. The DNA and ribosomes are used to synthesize some of its proteins (3).

        The mitochondrion is the location of the tricarboxylic acid cycle (TCA), production of ATP, and oxidative phosphorylation.  In the TCA cycle, pyruvate is oxidized and cleaved to form CO2 and acetyl-coenzyme A (acetyl-CoA), an energy-rich molecule. After a series of reactions on acetyl-CoA, NADH and FADH2 are formed, which are both electron carriers. This reaction also yields four ATP molecules. The electron carriers formed in the TCA cycle are active players in the electron transport chain, as electrons are transferred to acceptors such as oxygen. The electron transport chain involves an energy gradient within the inner membrane of the mitochondria in eukaryotes and in the plasma membrane in prokaryotes. In this process, NADH is oxidized to NAD+, while the electrons are transferred to other molecules (such as oxgygen) with more positive reduction potentials. Oxidative phosphorylation is the result of the electron transport chain, in which protons move across the mitochondrial membrane and ultimately produce a maximum of 34 ATPs. These processes are very simplified, as more complex explanations involve in-depth biochemistry (3).

         Through these complicated processes in the mitochondria, eukaryotic cells are able to reap the benefits of an abundant amount of energy to sustain more complex forms of life. Although the TCA cycle and electron transport chain produce small amounts of ATP, oxidative phosphorylation allows for 34 molecules of ATP to be produced.

Mitochondria and the Body

An eye that has been affected by optic neuropathy.
          We already have an idea of how beneficial mitochondria are to sustaining life, but what happens when mitochondria start to malfunction? As already mentioned, mitochondria contain their own DNA. Mitochondria are passed from mother to offspring in the cytoplasm of the egg. Over 200 human diseases are caused by mutations in DNA due to mitochondrial DNA’s inability to repair, unlike nuclear DNA. Most of these diseases come about in cells that require an abundance of ATP, such as muscle and nerve cells. Several examples of dysfunctional mitochondria-caused diseases are the following: optic neuropathy, often resulting in blindness; neurogenic muscle weakness; maternal and cardiomyopathy; and myoclonic epilepsy (2). Regardless of the primitive bacteria-eukaryotic cell relationship, it is apparent that eukaryotic cells have become very dependent on mitochondria to sustain life. 


    (1) The Endosymbiotic Theory. (2004, February 18). Retrieved from
    (2)    Brooker, R. J. (2009). Genetics: Analysis & Principles. (4 ed., pp. 119-120). New York: McGraw Hill. Print.
    (3)  Willey, Sherwood, and Woolverton. (2008).  Microbiology.  (7 ed., pp. 88 and 476-478). New York: McGraw Hill. Print.

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