Microbiomes are the beneficial microbial communities associated with plants and animals. We all have them and they influence everything about their host from development and fitness to reproduction. Needless to say, microbes are a huge driving force in the evolution of higher organisms.
The microbiome that most concerns humans is the one in our guts, and which primes our immune systems, helps us digest our food and protects us against infection. We acquire some of our ‘good bacteria’ from our mums when we pass through the birth canal but many of the bacteria found in our guts are obligate anaerobes which are killed by exposure to air. So how do they get from mother and child?
Recently it has been suggested that bacteria may actually migrate from the mothers gut to the mammary glands and be transmitted directly to babies through her breast milk. A paper just published in Environmental Microbiology provides the first direct evidence for this ‘mother-neonate direct transfer’ model.
The authors used culture dependent and independent methods to examine the microbes present in the faeces (poo to you) of mums and their newborn babies (neonates) and in the mum’s breast milk. They found the same species in all three samples for mother-baby pairs and the highest evidence for direct transfer was for strains of bifidobacteria, the Y shaped “good bacteria” that are added to probiotic drinks and yoghurts.
Although this study was carried out in collaboration with Nestle (who have a big line in probiotics) it is backed up by other recent studies and it certainly makes a lot of sense. Exactly how the bacteria get from the mother’s gut to the breast milk remains mysterious but expect rapid progress to be made in figuring this out. And remember, breast really is best.
I’ve been fascinated by lichens since I studied them on a biology field trip to Pembrokeshire many moons ago (geeky, I know). Although they look like weird plants that only grow in barren rocky landscapes they are actually microrganisms. Or rather, they are a collection of symbiotic microorganisms; a fungus and a cyanobacterium or green algae colonised by lots of other bacteria. They have been around for 600M years!!
A new study reportsthat lichens make a class of antibiotic called pederins only previously seen in bacterial symbionts of Paedurus beetles. The researchers used metagenomics (sequencing all of the DNA from all of the microorganisms in the lichen at the same time) and then looked at this big mix of DNA to see if they could find any genes involved in making antibiotics. Voila, they found a gene cluster for a pederin-type compound and then purified it, solved the structure and called it nosperin. This work is exciting because it suggests some antibiotics may be specific to symbionts, even when they are distantly related (in this case, beetles and lichens)!
It also suggests that the lichen symbiosis, like others we have written about (e.g. fungus growing ants and marine sponges), could be a source of novel antibiotics. So lichens might provide us with yet another untapped and unusual niche for natural product discovery which could eventually mean new antibiotics and new anticancer compounds in the clinic (hurray!). For me at least, this will be easier than sampling the marine environment, because we don’t have any submarines where I work.
Kapma et al (2013). Metagenomic natural product discovery in lichen provides evidence for a family of biosynthetic pathways in diverse symbionts. Proc Natl Acad Sci USA Early Edition doi: 10.1073/pnas.1305867110
What are a group of genes that help Mycobacterium tuberculosis infect mammalian cells doing in a harmless soil bacterium? Dr Paul Hoskisson explains his recent research, which is helping us understand the evolutionary roots of disease.
Scientists invest a lot of time and resources in trying to understand how bacteria cause disease. Generally, this involves studying a particular gene, or group of genes, in a pathogenic (disease-causing) bacterium to see what function it has during the infection process. In my laboratory, we have been trying to understand the evolutionary processes that cause these genes to develop.
Bacteria need some specialist skills if they’re going to cause disease: they must avoid being destroyed by the immune system, enter and multiply within host cells, and produce toxins. Bacteria have been around on Earth a lot longer than humans, which suggests that the genes needed to cause disease in humans have either evolved recently and rapidly (in evolutionary terms) or been co-opted from existing genes in harmless bacteria.
We noticed that the soil bacterium Streptomyces coelicolor has a cluster of genes that are very similar to pathogenicity genes present in Mycobacterium tuberculosis, the causative agent of tuberculosis. Other work has shown that these genes, known as mce (mammalian cell entry) genes, are used by M. tuberculosis to colonise and survive inside human immune cells called macrophages. We disrupted these genes in S. coelicolor to see what happened.
As the mce genes are used by M. tuberculosis to infect and survive in macrophages, we wanted to see what happened to the mce-deficient S. coelicolor mutants under similar conditions. However, because S. coelicolor lives in the soil, it rarely encounters any immune cells, so we had to get creative.
Rather than use immune cells, we used amoebae. This might not seem like an obvious choice, but these single-celled organisms are eukaryotic, just like immune cells, and engulf bacteria in a similar way. We got a strange result when we fed the S. coelicolor mce mutants to the amoebae: the amoebae all died (see image above). This effect has been seen in M. tuberculosis as well – mce mutants are hyper-virulent and much better at killing immune cells than regular M. tuberculosis. This is counterintuitive, but while the mutant M. tuberculosis strain may be excellent at killing macrophages, it is unable to cause disease in a whole animal – presumably because of the presence of the complete immune system, which is much more complex.
We did a little detective work and discovered that the mce genes encode a transporter that bacteria use to take up sterol (a type of fat), which they can use as a source of food, from the environment. It is thought that M. tuberculosis uses this transporter to take up sterols because other nutrients are hard to find inside macrophages.
One location where Streptomyces encounters sterols in the environment is around the roots of plants, an environment known as the rhizosphere. We showed that the S. coelicolor mce mutant is poorer at colonising plant roots than the wild-type S. coelicolor, which suggests that sterols are an important carbon source for these bacteria.
We suggest that as these bacterial species adapted to their particular environment – soil in the case of the Streptomyces and human immune cells for M. tuberculosis – their respective mce genes evolved to operate under the different conditions. Understanding how the selection process has led to the changes in function are essential to our appreciation of the evolution of virulence in bacteria and could significantly aid our understanding of the emergence of pathogenic bacterial strains.
Paul A Hoskisson is a lecturer in microbiology at the University of Strathclyde. His research focuses on antibiotic-producing actinomycetes and emerging actinomycete pathogens.
Image adapted from the original article published in Scientific Reports article under the Open Access license.
Clark LC et al. Mammalian cell entry genes in Streptomyces may provide clues to the evolution of bacterial virulence. Sci Rep 2013;3:1109. doi:10.1038/srep01109
Bacterial cells are surrounded by a highly cross-linked cell wall that has to be constantly broken down and remade as the cells get bigger. Since most bacteria reproduce by dividing the cell into two they also have to build a new bit of cell wall in the middle of the cell to make two daughter cells. In bacteria the FtsZ protein forms a Z ring to mark this site of cell division and all the other cell division proteins assemble on this Z ring and remodel the cell wall.
Despite this, it has been known for a long time that some bacteria can exist as L forms which have lost their cell wall. Even more amazing, these L-form bacteria don’t need FtsZ to divide and instead they just bud off membrane vesicles, some of which contain DNA and enough proteins to form a new cell.
Jeff Errington’s group in Newcastle recently made stable L forms of a bacterium called Bacillus subtilis, effectively reversing 3 billion years of evolution . These bacteria can live without a wall or FtsZ but they still need a cell membrane to contain the cell contents and in another groundbreaking paper Jeff’s group have shown that simply increasing the amount of membrane the cell makes is enough to make these L-forms divide.
The beauty of these L forms is that they help us to understand how the first living cells, reproduced themselves around 4 billion years ago. In the absence of a cell wall and a complicated cell division machinery they simply increased their surface area to volume ratio in order to propagate. And that, frankly, is amazing.
Mercier R, Kawai Y and Errington J (2013). Excess membrane synthesis drives a primitive mode of cell proliferation. Cell 152 997-1007.
Image credit: The Red Lexicon on Wikimedia Commons
Posted by Matt Hutchings
This isn’t a research blog as such, just an attempt to get everyone to read a new perspective article entitled “Animals in a bacterial world”. Here at microbelog we’ve been banging on about how important symbioses between bacteria and eukaryotes are for a quite a while now. So imagine our excitement to read this article in the latest issue of the Proceedings of the National Academy of Sciences USA. Although slightly evangelical (or as one of my evolutionary biologist colleagues put it “messianic”), this is well worth a read. It’s also good to see Carl Woese and Lynn Margulis, both of whom sadly passed away recently, getting the credit they deserve. Facts like one third of human DNA is bacterial in origin is the kind of thing that gets us very excited! This is a call to arms and it’s certainly never been a more exciting time to be a microbiologist!
Image credit: Picture of a captive leaf-cutter ant colony taken by Andrew Smith, John Innes Centre, Norwich 2012.
Recently, I found a paper published in mBIO that describes how antibiotic use in farming is involved in the spread of resistance genes. In this case the work focuses on the humble honeybee (Apis mellifera). Since the 1950s, beekeepers in the USA have been using the antibiotic oxytetracycline – a ‘broad-spectrum’ antibiotic that kills most species of bacteria – to prevent infections that can cause ‘foul brood’, a disease that kills bee larvae. As you can imagine, using a single antibiotic for more than 50 years has led to some selective pressure. In this work, researchers from Yale University were investigating the prevalence of disease resistance in bee gut bacteria.
This might seem like a strange place to look, but it actually has its advantages. Unlike the supremely complex ecosystem of the human gut microbiome, the bee’s is pretty simple, with eight species making up over 95% of the gut bacteria in adult worker bees. The small number of species and the knowledge of how hives have been treated allowed the researchers to monitor the impact of decades of antibiotic use.
Sometimes you find a paper with a title so intriguing you just have to find out a little more about it. Recently, I came across a paper about ‘entombed pigs’, so how could I possibly ignore it? I learned a fair bit about animal-disease control methods in Asia and the use of quicklime to decompose corpses , a fairly standard weekend for me.
The work centres on foot-and-mouth disease (FMD), a viral infection of hoofed animals caused by Aphthovirus. It causes significant suffering in animals and has serious economic consequences: a 2001 outbreak is estimated to have cost the UK £8 billion.
Millions of infected animals were culled in South Korea in 2010/11, then buried (rather than burnt, as they are in the UK). The slaughtered animals were placed in five-metre-deep pits and covered with quicklime and copious amounts of soil to prevent the FMD spreading. Problem solved? Well, perhaps not.