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Tag: mitochondria

Life without Oxygen

No, that’s not a reference to a Jordin Sparks/Chris Brown song, its the theme for the paper of the month.

imageThis month, in expression of my gratitude to the kind folks at Open Access publisher BioMedCentral for sending me a “clone” of their very adorable mascot Gulliver (picture left), I have decided to do a post spotlighting a very interesting BMC Biology paper on the discovery of metazoans (creatures in the Animal Kingdom) which live in environments completely devoid of oxygen.

The researchers began their quest by looking at the L’Atalante basin (see below), a so-called deep hypersaline anoxic basin (DHAB) in the Mediterranean Sea. The area in question is over 3 km deep, and is rich in hydrogen sulfide and nearly saturated with salt, the result of which prevents oxygen from less salty waters from mixing into the anoxic (without oxygen) zone.


Now, scientists have known about single-celled bacteria and protozoans capable of living without oxygen for quite some time – and so they were expecting to find tons of those in the anoxic sediments in L’Atalante. What they were hoping to find, however, were multicellular animals capable of living permanently there as well. And find them they did. The researchers, in sifting through the sediment, were able to find three species of living, microscopic (~1 millimeter in size, see below) Loriciferans (themselves a newly discovered, but highly diverse set of creatures).


After verifying that they were alive (and not just dead Loriciferans who sank from another layer of water) and able to do basic things like metabolism without air (and not just air-breathers who were “visiting” the anoxic sediments), the researchers set out to try to determine how these Loriciferans were able to survive:

  • without oxygen
  • in such a toxic environment (Hydrogen Sulfides are strong reducing agents)
  • in an environment as salty as the DHAB

Although the researchers didn’t answer these questions with the level of rigor I would have liked to see, they did make two interesting observations which suggest the sorts of adaptations these creatures evolved to cope:

  • Chemical composition of their bodies: The researchers were able to show (see table below) that Loriciferans from the L’Atalante DHAB had higher levels of Magnesium, Silicon, Iron, and Bromine then their non-anoxic cousins, but lower levels of Calcium, Copper, and Zinc. While this wasn’t completely explained, one might hazard a guess that to survive the harsh environment, these Loriciferans evolved new body structure which used different elements to help cope with/shield themselves from the harsh exterior.
  • No mitochondria, only hydrogenosomes: Almost all oxygen-breathing cells have little organelles in them called mitochondria. Mitochondria are responsible for using oxygen to help convert metabolic products into energy cells can consume. When the researchers applied an electron microscope to the cells of these oxygen-free Loriciferans, they were unable to find any mitochondria. Instead, they found an abundance of hydrogenosome-like structures (below, see all the “H”’s). Hydrogenosomes have previously been found in single-celled creatures which live without oxygen. They use hydrogen, instead of oxygen, to help a cell get energy. This is the first time hydrogenosome-like structures have been found in a multi-cellular creature and probably are a vital adaptation for the Loriciferans in order to let them survive in the DHABs.

Found 3 new species of animal life capable of surviving without oxygen? Sounds like a naturalist’s dream come true. But where does one go from here? From my perspective, I’m most interested in two things.

The first is an extension of the studies the researchers conducted on how these creatures have been able to survive. Identifying “hydrogenosome-like organelles” and high-level “chemical/structural adaptations” is cool, but unsatisfying for anyone trained in basic biology. I want to understand how similar those hydrogenosome-like structures are to hydrogenosomes from single-celled creatures. I want to know what genes are responsible for the hydrogenosome-like structures. I want to understand what the different chemical and structural adaptations do!

The second area of investigation is ecological in nature. What exactly does the food web look like down there? Its great that we’ve found single-celled and multi-cellular creatures, but how do they interact?

Paper: Danovaro, Roberto et al. “The first metazoa living in permanently anoxic conditions.” BMC Biology 8:30 (6 Apr 2010) – doi:10.1186/1741-7007-8-30

(Image credit – Gulliver’s Facebook page) (Figures from Additional File 1, Figure 1, Additional File 4, Figure 4 of paper)

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Collateral Damage by Mitochondria

Another month, another paper to read and blog about.

This month, I read a paper (HT: my ex-college roommate Eric) by a group from Beth Israel about systemic inflammatory response syndrome (SIRS) following serious injury. SIRS, which is more commonly understood/found as sepsis, happens when the entire body is on high “immune alert.” In the case of sepsis, this is usually due to an infection of some sort. While an immune response may be needed to control an internal infection, SIRS is dangerous because the immune system can cause a great deal of collateral damage, resulting in potentially organ failure and death.

Whereas an infection has a clear link to sepsis, the logic for why injury would cause a similar immune response was less clear. In fact, for years, the best hypothesis from the medical community was that injury would somehow cause the bacteria which naturally live in your gut to appear where they’re not supposed to be. But this explanation was not especially convincing, especially in light of injuries like burns which could still lead to SIRS but which didn’t seem to directly affect gut bacteria.image

Zhang et al, instead of assuming that some type of  endogenous bacteria was being released following injury, came up with an interesting hypothesis: it’s not bacteria which is triggering SIRS, but mitochondria. A first year cell biology student will be able to tell you that mitochondria are the parts of eukaryotic cells (sophisticated cells with nuclei) which are responsible for keeping the cell supplied with energy. A long-standing theory in the life science community (pictured above) is that mitochondria, billions of years ago, were originally bacteria which other, larger bacteria swallowed whole. Over countless rounds of evolution, these smaller bacteria became symbiotic with their “neighbor” and eventually adapted to servicing the larger cell’s energy needs. Despite this evolution, mitochondria have not lost all of their (theorized) bacterial ancestry, and in fact still retain bacteria-like DNA and structures. Zhang et al’s guess was that serious injuries could expose a mitochondria’s hidden bacterial nature to the immune system, and cause the body to trigger SIRS as a response.

Interesting idea, but how do you prove it? The researchers were able to show that 15 major trauma patients with no open wounds or injuries to the gut had thousands of times more mitochondrial DNA  in their bloodstream than non-trauma victims. The researchers were then able to show that this mitochondrial DNA was capable of activating polymorphonuclear neutrophils, some of the body’s key “soldier” cells responsible for causing SIRS.

The figure above shows the result of an experiments illustrating this effect looking at the levels of a protein called p38 MAPK which gets chemically modified into “p-p38” when neutrophils are activated. As you can see in the p-p38 row, adding more mitochondrial DNA (mtDNA, “-” columns) to a sample of neutrophils increases levels of p-p38 (bigger, darker splotch), but adding special DNA which blocks the neutrophil’s mtDNA “detectors” (ODN, “+” columns) seems to lower it again. Comparing this with the control p38 row right underneath shows that the increase in p-p38 is likely due to neutrophil activation from the cells detecting mitochondrial DNA, and not just because the sample had more neutrophils/more p38 (as the splotches in the second row are all roughly the same).

Cool, but does this mean that mitochondrial DNA actually causes a strong immune response outside of a test tube environment? To test this, the researchers injected mitochondrial DNA into rats and ran a full set of screens on them. While the paper showed numerous charts pointing out how the injected rats had strong immune response across multiple organs, the most striking are the pictures below which show a cross-section of a rat’s lungs comparing rats injected with a buffer solution (panel a, “Sham”) and rats injected with mitochondrial DNA (panel b, MTD). The cross-sections are stained with hematoxylin and eosin which highlight the presence of cells. The darker and “thicker” color on the right shows that there are many more cells in the lungs of rats injected with mitochondrial DNA – most likely from neutrophils and other “soldier cells” which have rushed in looking for bacteria to fight.

Amazing isn’t it? Not only did they provide part of the solution to the puzzle of injury-mediated SIRS (what they used to call “sterile SIRS”), but lent some support to the endosymbiont hypothesis!

Paper: Zhang, Qin et al. “Circulating Mitochondrial DAMPs Cause Inflammatory Responses to Injury.” Nature 464, 104-108 (4 March 2010) – doi:10.1038/nature08780

(Image credit) (Figure 3 and 4 from paper)