mBiosphere

Dead vent, thriving habitat: expired hydrothermal chimneys home to plenty of bacteria

Hydrothermal chimneys can be found wherever you have a mid-ocean ridge spreading center. Like geysers on the sea floor, chimneys are formed when hot, mineral-laden sea water emerges from beneath the crust and deposits those minerals in a (sometimes towering) column rich in metals and sulfur. (The one pictured at the right is 9 meters tall.) Microbiologists have studied these chimneys for a while now, examining which bacteria and archaea predominate and what they might be doing while the gushers flow, but a group at the University of Southern California and the University of Minnesota, Twin Cities have taken a look at the communities that exist on chimneys that have long since plugged up and stopped - dormant chimneys, referred to as "inactive sulfides". They found some telling differences between the communities on active chimneys and the ones on chimneys that no longer flow - differences that show inactive chimneys are actually active biogeochemical engines that continue to cycle sulfur, nitrogen, and iron on the ocean floor.

The changeover to becoming a non-productive vent is a significant one, says Katrina Edwards, the senior author on the study. When a chimney stops spouting sea water, "the chemistry [of the chimney] goes from being dominated by fluid emissions - venting of hydrothermal fluids that are not in equilibrium with bottom seawater - to a mineral-chemistry based system" says Edwards. So, active chimneys are dominated by reactions between materials in venting sea water and the surrounding sea water and dormant chimneys are dominated by reactions between sea water and the minerals in what is left of the chimney.

This makes for a big difference in habitats, differences that are reflected in the 16S rRNA sequences of the organisms they find in these two types of chimney. One glaring difference is the ε-proteobacteria and Aquificae: the predominant groups on active chimneys, they are rare on inactive chimneys, where they are probably replaced by α-, β-, δ-, and γ proteobacteria and Bacteroidetes, which seem to thrive there and probably participate in redox transformations of sulfur, nitrogen and iron. Other observations also indicate the communities are undergoing ecological succession, in which old species and processes are slowly replaced by others.

And how long have these chimneys been dormant while the accompanying bacterial communities are busy chugging away within? Co-author Jason Sylvan says they don't know the age of their particular sample sites, but that others working at the 9°N East Pacific Rise site have used lead isotope ratios to date the dormant features in the area from several decades to 20,000 years old.

"Given that the structures persist for thousands of years," says Sylvan, "all the while supporting active microbial communities, it is certainly possible that these communities have an impact on ocean chemistry."

Edwards hopes to do continue her work with the chimneys. "The deposits that are created through hydrothermal venting are poorly understood over long time frames. We know they stick around for multiple decades, but what influence they have on biological and chemical oceanographic processes is uncertain."

How does E. coli attack human RhoGEFs without hurting its own RhoGEFs?

Enteropathogenic Escherichia coli and enterohemorrhagic E. coli (EPEC and EHEC, neither of which you want in your hamburger) deploy a powerful weapon against human cells: the effector EspH binds to human Rho guanine exchange factors. RhoGEFs are important controls on Rho, which, in turn, is responsible for many cellular processes. Targeting RhoGEFs is an easy way to cause a lot of problems, kind of like dropping a grenade in an important cellular control room.

But E. coli has its own RhoGEFs, so how does the pathogen get away with this attack? A study in mBio this week reveals E. coli gets round this problem with RhoGEFs that are resistant to its attacks, but that's not the end of the story. E. coli also translocates its own bacterial RhoGEFs into human cells to hijack cellular machinery for its own benefit.

Gut Bacteria in Autistic Children Differ From Non-autistic Children

Individuals with severe autism often suffer from another problem as well: gastrointestinal disturbances. The underlying reason for this apparent link is unknown, but a study in mBio this week reveals that the guts of autistic children differ from other children in at least one important way: many children with autism harbor a genus of bacteria in their guts that non-autistic children do not.

Earlier work has revealed that autistic individuals with gastrointestinal symptoms often exhibit inflammation and other abnormalities in their upper and lower intestinal tracts. However, scientists do not know what causes the inflammation or how the condition relates to the developmental disorders that characterize autism. Williams et al. show that the guts of autistic children with gastrointestinal problems are often home to species of Sutterella, a genus with few cultivated representatives. Whether or not these bacteria are a cause or effect of autism remains to be seen.

"The relationship between different microorganisms and the host and the outcomes for disease and development is an exciting issue," says Christine A. Biron of Brown University and editor of the study. "This paper is important because it starts to advance the question of how the resident microbes interact with a disorder that is poorly understood," says Biron.

Ribosomal RNA sequences belonging to the genus Sutterella represented a relatively large proportion of the microorganisms found in 12 of 23 tissue samples from the guts of autistic children, but sequences from these organisms were not detected in any samples from non-autistic children. Why this organism is present only in autistic kids with gastrointestinal problems and not in unaffected kids is unclear.

"Sutterella has been associated with gastrointestinal diseases below the diaphragm, and whether it's a pathogen or not is still not clear," explains Jorge Benach, Chairman of the Department of Microbiology at Stony Brook University and a reviewer of the report. "It is not a very well-known bacterium," says Benach.

In children with autism, digestive problems can be quite serious and can contribute to behavioral problems, making it difficult for doctors and therapists to help their patients. Autism, itself, is poorly understood, but the frequent linkage between this set of developmental disorders and problems in the gut is even less so.

Benach says the study was uniquely powerful because they used tissue samples from the guts of patients as opposed to stool samples. "Most work that has been done linking the gut microbiome with autism has been done with stool samples," says Benach, but the microorganisms shed in stool don't necessarily represent the microbes that line the intestinal wall. "What may show up in a stool sample may be different from what is directly attached to the tissue," he says.

Tissue biopsy samples require surgery to acquire and represent a difficult process for the patient, facts that underscore the seriousness of the gastrointestinal problems many autistic children and their families must cope with.

Benach emphasizes that the study is statistically powerful, but future work is needed to determine what role Sutterella plays, if any, in the problems in the gut. "It is an observation that needs to be followed through," says Benach.

Commentary: Toxoplasma history is complicated

A Commentary in mBio this week discusses the impact a paper published in November has had on our understanding of the biogeography of Toxoplasma gondii. The parasite, distributed worldwide, has a more complicated family tree than previously suspected, and a crucial chromosome called Chrla is sprinkled around otherwise highly divergent strains. Walzer and Boyle say it now seems likely that the chromosome was introduced into North America from South America rather than the other way around.