Wetland restoration: Is it worth the effort?

If forests are the lungs of our planet, then wetlands are surely the liver. Wetlands filter overland runoff through a unique suite of plants and soil microorganisms that break down harmful compounds, ensuring that waters reaching streams and coastlines are contaminant-free. Wetlands also store a massive amount of carbon in their soils, serve as a nursery ground for many fisheries, and protect shorelines from floods and storm surges.

Despite these benefits and more, humans allowed worldwide wetland degradation to continue unchecked for two hundred years. Instead of protecting existing wetlands, we gamble on restoration efforts, investing over $70 billion to bring back functional wetlands in North America alone. Until now the overall outcome remained unclear. But after investigating 621 wetland restoration projects around the world, a team of scientists led by Dr. David Moreno-Mateos and renowned ecologist Dr. Mary Power of the University of California Berkeley determined that wetland restoration is generally a losing bet. They published their results last month in PLoS Biology.

The team combed the scientific literature for studies that compare restored and newly created wetlands to adjacent undisturbed wetlands. They compiled all the data from these studies to find out how three characteristics of the restored or created wetlands recover over time: hydrology, biological community, and biogeochemistry.

Wetland hydrology includes water level, flooding patterns, and water storage. It recovers quickly because it depends on the surface features engineered by restoration teams. Before they place a single plant in the ground, restoration teams manipulate soil levels and permeability to achieve ideal patterns of wetland hydrology. The biological community, however, is much harder to recreate. Even after 100 years, biological communities in restored wetlands only recovered to 77% of their undisturbed counterparts. Moreover, plant communities recovered more slowly than animals.

Biogeochemistry, the movement and transformation of nutrients in a system, only recovered to 74% after 50 to 100 years. A healthy, functioning wetland stores large amounts of carbon and organic matter, because their flooded soils deprive decomposing microorganisms of necessary oxygen. If wetlands dry out during a disturbance, oxygen reaches decomposers, allowing them to break-down carbon compounds and larger pieces of organic matter. The decomposers eventually release carbon dioxide to the atmosphere as a byproduct of this process. Once restoration teams restore the proper wetland hydrology, decomposition shuts down and carbon begins to build up in the soil once again. However, even after twenty years, the amount of carbon and organic matter stored in wetland soils remains significantly less than levels in undisturbed wetlands.

Dr. Power's team suggests that restored wetlands do not resemble their original condition because they have shifted to alternative states. Much like building a house, successful ecosystem restoration requires that all the right pieces come together in the correct order. If a construction crew lays out the wrong foundation or neglects to build the second floor, the house will look completely different from the blueprints. The result of this botched construction project is like an alternative state. In ecosystems, the presence or absence of certain organisms determines which organisms come next. If a restoration team fails to introduce an important organism, or does so at the wrong time, a restored wetland may give rise to an alternative state that differs from the goal.

When it comes to wetland restoration, we may know which plant species to add, but the proper foundation remains unknown. Wetland plant communities and biogeochemistry depend on soil microorganisms. If the microorganism community shifts during wetland degradation, or if restoration requires imported soils, the soils may lack the microorganisms necessary for native wetland plants to grow. These unseen changes underground have cascading effects through the wetland ecosystem, producing an alternative state. Alternative states often host different organisms, function at reduced levels, and cannot confer the ecosystem benefits we depend on. Unfortunately, the only way to fix it is to start again from scratch.

Moreno-Mateos D, Power ME, Comı´n FA, Yockteng R (2012) Structural and Functional Loss in Restored Wetland Ecosystems. PLoS Biol 10(1): e1001247. doi:10.1371/journal.pbio.1001247

Photo: Vermont Department of Forests, Parks and Recreation

The ocean's most exclusive community.

The great thing about science is that questions lead to answers. The bad thing is that through this process, a subject that was once novel and strange slowly loses its mystique. When the thrill is gone and the mysterious becomes mundane, the jaded biologist longing for that delicious scientific buzz need only look down - way way down. And, oh my GOODNESS, a really thrilling bit of science was just pulled up from the uncharted ocean depths and published in PLoS Biology.

Deep-sea hydrothermal vents! Is there anything more amazing? They are remote like outerspace but with thriving communities of freaky biota. And as a team of researchers, led by Dr. Alex Rogers of Oxford University, recently found – if you’ve seen one you have NOT seen them all.

These ecosystems are so mystifying because they are fundamentally different from the ecosystems we are used to seeing. Whether you are in tropical rainforest, arctic tundra, or open ocean, nearly all food webs are built upon the plants and algae that harness sunlight to transform carbon dioxide into organic molecules. Photosynthesis is incredible, but also pedestrian. Things get really strange when you look into the darkness and find bizarre organisms that have capitalized on a different energy source – poisonous, smelly hydrogen sulfide gas.

Deep-sea hydrothermal vents, found at an average depth of 2100 meters, spew plumes of hot water from the earth’s crust. This water can be as hot as 400˚C and contains high concentrations of hydrogen sulfide. The surrounding water is nearly freezing and dark as night with pressures so great it keeps the hot plumes from boiling. Still some organisms have managed to thrive in this oppressive environment. Not surprisingly, it all comes down to the microbes. Bacteria and archaea living in and around the vent utilize the energy stored in the bonds of hydrogen sulfide to fix carbon dioxide into organic molecules. This process, known as chemosynthesis, was only a theory until it was observed in action at the hydrothermal vents of the Galapagos Ridge in 1977.

The unusual properties at the base of the vent food web radiate up through all the animals it supports. The giant tube worm that hosts chemosynthetic bacteria within its body is the most familiar image. In many ways it has assumed the role of the community’s iconic species. That is until Dr. Rogers and his team restored the mystique of the hydrothermal vent ecosystem.

Departing from the vents of the tropics and subtropics that are relatively easy to access, the team examined the communities on the East Scotia Ridge (ESR), 500 km to the east of Cape Horn between South America and Antarctica. At a depth of more than 3000 meters in the Southern Ocean, the ESR has two ridge segments with hydrothermal activity, E2 and E9. A deep-sea drive by the remotely operated vehicle Isis revealed that these areas are completely devoid of the tubeworms, polychaetes, clams, and shrimp that we’ve come to expect in hydrothermal vent communities. Rather, they host a complex community of endemic organisms – organisms that haven’t been seen anywhere else – notably a new species of crab, stalked barnacles, limpets, snails, sea anemones, and a seven-armed starfish.

The biological diversity of these areas is built upon the diverse landscape. In some spots chimneys as tall as 15 meters release concentrated plumes of mineral-rich water from the Earth’s crust. This water emerges at temperatures exceeding 300˚ C, and when it hits the near-freezing water of the ocean floor, the minerals fall out of solution and create that black smoker appearance. In other areas there is more diffuse vent flow with temperatures closer to the surroundings. Even between the two sites there is variation in the chemical composition of the vented liquid. These differences could affect the microorganism populations at the two sites which would have cascading affects up the food web.

The truly thrilling thing about the ESR discovery is not the strange biota, because, let’s be honest – finding new species in a remote habitat is old hat. The amazing thing is WHY the species are so strange and why the ESR community is different from the ones we see in similar ecosystems. While they seem inhospitable to us, hydrothermal vents are the only suitable habitat for these organisms. In that way they are just like islands out at sea or parks in an urban landscape. Biogeography is the study of species distributions across space – the traits of an organism that lead it to new areas and the barriers that stand in its way. And remarkably, when you consider all the geologic, hydrologic, and biologic pieces of the puzzle, it appears that hydrothermal vent communities suggest the same patterns of biogeography that govern terrestrial communities.

Deep ocean organisms face unimaginable hurdles to dispersal. Larvae might catch a ride on an ocean current, but many of them won’t last long before passing by another hydrothermal vent. These vents are found only at the boundaries of tectonic plates, which would serve as a great dispersal corridor if they corresponded with the currents. They don’t. Even more daunting is the surface to sea-bed Polar Front, which encloses the Southern Ocean and effectively blocks the entry of outside organisms. At the Polar Front water temperatures and salinity levels change abruptly, creating an insurmountable physiological challenge to most organisms attempting to cross. Knowing this it’s really no shock that the ESR has so many endemic species and so few of the usual suspects. With these barriers preventing migration, the populations of the ESR have been held in reproductive isolation for millions of years with the forces of evolution at work.

However, over geologic time scales ocean currents and plate movements are not even constant, which adds a whole new twist to the story! The hydrothermal vents appeared when the ESR began to spread – around 15 million years ago. That period corresponded with climatic conditions that made the Polar Front less intense, meaning that organisms dispersing from other vent communities actually had a chance to colonize this brand new environment. But the gates closed around 13.8 million years ago when the climate changed and the Polar Front strengthened.

Even more interesting is the phylogenetic history of one of the ESR endemics, which seems to corroborate the geologic and climatic stories. A new species of Kiwa crab, found in the vents of the ESR, is closely related to K. hirsuta of the nearby Pacific Antarctic Ridge. By looking at differences in their genetic markers, researchers loosely estimated that the two species diverged around 12.2 million years ago. Other ESR animals show similarity to species found in hydrothermal vents in the lower latitudes of both the Atlantic and Pacific. The dispersal of organisms from two oceans was likely aided by the Antarctic Circumpolar Current, which circulates around Antarctica, linking the Atlantic, Pacific, and Indian Oceans.

Dr. Rogers' team’s research adds another layer of complexity to the biogeography of vent ecosystems, even suggesting that the Antarctic vents comprise a new biogeographic province. For scientists and non-scientists alike it represents a whole new world of mysteries to be revealed, recharging our hope for big, exciting discoveries.

Rogers AD, Tyler PA, Connelly DP, Copley JT, James R, et al. (2012) The Discovery of New Deep-Sea Hydrothermal Vent Communities in the Southern Ocean and Implications for Biogeography. PLoS Biol 10(1): e1001234. doi:10.1371/journal.pbio.1001234

Silencing a mysterious cellular passenger.

Malaria is an ancient killer. For millennia it has claimed the lives of the world’s most vulnerable populations - the youngest and the poorest. Despite the human species' long history with the disease, it remains a mystery to us in many ways. We really only know the basics. Plasmodium falciparum, the parasitic microorganism that causes malaria, has an incredibly complex lifecycle. It is transmitted to humans in the saliva of a tiny Anopheles mosquito. When the mosquito bites, the parasites flow into the bloodstream. Once inside a human, the parasite goes through multiple phases, taking residence in liver cells and red blood cells. In each phase it feeds on the resources within the human cell as it grows rapidly and replicates its cellular machinery many times. Then it suddenly divides into many new individuals, aggressively bursting out of the human cell. This parasitic amplification occurs once in a liver cell, and subsequent to its forceful exit from the liver, it will amplify many times in red blood cells.

Not only does the Plasmodium undergo a very complicated lifecycle, it also contains some unusual cellular equipment. The Plasmodium contains a plastid, an organelle like the chloroplasts found in plants, which is capable of photosynthesis. What could a plastid be doing inside a human parasite? This question has managed to elude researchers for twenty years. One thing we know for sure is that it’s not performing photosynthesis like its chloroplast brethren.

The plastid found in Plasmodium is called an apicoplast. It is believed that plastids were once free-living bacteria that were gobbled up by algae 1500 million years ago and harnessed for their photosynthetic ability. Like all complex plastids, the apicoplast found its way into the Plasmodium eons ago when a Plasmodium engulfed a single-celled red algae that contained plastids. Over millions of years of evolution, however, the Plasmodium’s plastid passenger has lost its photosynthetic power and shipped most of its genetic information to the nucleus of the Plasmodium. In many ways the apicoplast seems like nothing more than an evolutionary relict. However, if the apicoplast serves any critical functions for the Plasmodium, it could be a key target for anti-malarial treatments.

Scientists have high hopes for apicoplast-targeted malaria treatments for one very important reason. Even though it has resided in more complex organisms for ages, the apicoplast is still of bacterial origin. In contrast, the Plasmodium, like a human cell, is a eukaryote. Definitions aside, this means that Plasmodium metabolism is more similar to metabolism in human cells than it is to apicoplast metabolism. Therefore, treatments that interrupt metabolic pathways of the apicoplast are likely to leave human cells unharmed, whereas treatments that target the Plasmodium itself may have the same adverse effect on human cells. This leaves scientists left to ponder the role of the apicoplast in the Plasmodium. What essential functions does the apicoplast perform for the Plasmodium that the Plasmodium cannot do for itself?

Both apicoplasts and human cells produce important molecules called isoprenoid precursors. The human and apicoplast versions of these molecules may look identical after synthesis, but since human cells are eukaryotic and apicoplasts are more like bacteria, the metabolic pathways that produce them are completely different. After the isoprenoid precursors are made in the apicoplast, they are shipped out into the parasite where they are used to make isoprenoids, a diverse and biologically important class of molecules. This step occurs during the blood stage of the parasite’s life cycle. Scientists believe that the synthesis and export of these isoprenoid precursors may be the only function of the apicoplast that is actually essential for parasitic growth.

In a recent publication in PLoS Biology, Drs. Ellen Yeh of Stanford and Joseph DeRisi of UCSF were able to demonstrate just how important these isoprenoid precursors are to the Plasmodium. It is known that several antibiotics are effective at combating malaria. Antibiotics attack the bacteria-like apicoplast, not the Plasmodium itself. However, their effectiveness at killing the malaria parasite suggests that functions of the apicoplast must be essential to the survival of the Plasmodium. Yeh and DeRisi took this information one step further, attempting to understand the mechanism of these antibiotics that cause the parasite to die.

They grew Plasmodium in a laboratory culture and treated the culture with antibiotics. As expected, the parasites stopped growing or died. Next they treated the cultures with antibiotics but added isoprenoid precursor molecules. By doing this they found that one particular molecule, IPP, “rescued” the Plasmodium in the culture. Even though the antibiotics killed the apicoplast, the Plasmodium survived with the addition of IPP. From this simple experiment, they were able to deduce that the essential function that the apicoplast performs for the Plasmodium is the synthesis of IPP.

Now that scientists have discovered the role of the apicoplast, they can target this metabolic function when developing new anti-malarials. In addition to that, through their experiment Yeh and DeRisi were able to produce a Plasmodium strain that lacks the apicoplast. This strain will be a powerful tool for Plasmodium studies, especially for identifying apicoplast drug targets and more advanced vaccines. Well done Dr. Yeh and Dr. DeRisi!

Yeh E, DeRisi JL (2011) Chemical Rescue of Malaria Parasites Lacking an Apicoplast Defines Organelle Function in Blood-Stage Plasmodium falciparum. PLoS Biol 9(8): e1001138. doi:10.1371/journal.pbio.1001138

The image comes from work by Waller, et al. (2000). This image shows the apicoplast, stained green, inside a Plasmodium during its many cellular stages in the blood phase. Notice that the apicoplast is replicated many times before the parasite divides into several new individual cells. The EMBO Journal (2000) 19, 1794 - 1802 doi:10.1093/emboj/19.8.1794

Be a good landlord.

Antibiotic-resistant superbugs are scary, but they are not the only negative, long-term consequence of our overuse of antibiotics. Dr. Martin Blaser of the Department of Medicine at NYU recently wrote commentary for Nature regarding the liberal use of antibiotics and its destructive impact on beneficial bacteria. Our gastrointestinal tracts provide habitat for a community of microorganisms that aid in digestion, produce vitamin K, and guard against harmful invaders. From an ecological perspective, these are mutualisms – relationships in which both organisms, the human and the bacterium, derive a benefit. This relationship should be protected. Instead, we cause irreparable damage the community of helpful bacteria with repeated courses of antibiotics. A therapeutic dose of amoxicillin may clear-up an ear infection, but not without collateral damage to these beneficial microbiota. Many people experience an upset stomach during a course of antibiotics. This is an indication that our helpful bacteria have been eliminated, but the results may go far beyond a tummy ache.

I spent some time in the Blaser Lab this summer where scientists and students were hard at work researching Helicobacter pylori. As Dr. Blaser explains in his essay, H. pylori was the dominant microbe in the stomachs of most people in the twentieth century. By the turn of the twenty-first century, however, fewer than 6% of children in the United States, Germany and Sweden were carrying the organism. H. pylori may have a bad rap for its connection to ulcers and stomach cancer, but its eradication has several surprising effects. For instance, people without the bacterium are more likely to develop asthma, hay fever, and skin allergies. Moreover, H. pylori helps regulate ghrelin and leptin, hormones that control appetite and metabolism, which may have implications in obesity. A dose of amoxicillin administered to treat a respiratory infection will also eliminate H. pylori in 20 – 50% of cases.

Farmers have noticed that repeated low doses of antibiotics cause animals to gain weight with less food. The Blaser lab has discovered that comparable sub-therapeutic doses cause changes in body fat and tissue composition in mice. Large doses, like those used to treat childhood infections, have similar results. Dr. Blaser goes on to emphasize the importance of age. The physiological changes that are triggered by antibiotic usage early in life are the hardest to reverse, yet the average child in the United States receives 10 – 20 courses of antibiotics before age 18.

To read more about threats to your friendly bacterial tenants and what we should do to protect them, read Dr. Blaser’s expert opinion in his essay for Nature.