Though less Fungal (and more fungal, if you’ll grant me that) than most of the stories we cover, a recent analysis of the Diplonema papillatum mitochondria genome sequence is interesting nonetheless. The genome consists of over 100 chromosomes, each roughly 6 kilobasepairs (kbp) or 7 kbp in size. However, each chromosome contains only a short (less than 500 bp) gene encoding region. It appears that genes are scrambled, where modular genetic units are dispersed across many chromosomes. Curiously, despite having discontigous genes, cDNA sequencing identifies contiguous and properly ordered mRNA. So just how are scrambled genes expressed and asssembled?
Few organisms are as well understood at the genetic level as Saccharomyces cerevisiae. Given that there are more yeast geneticists than yeast genes and exemplary resources for the community (largely a result of their size), this comes as no surprise. What is curious is the large number of yeast genes for which we’ve been unable to characterize. Of the ~6000 genes currently identified in the yeast genome, 1253 have no verified function (for the uninclined, this is roughly 21% of the yeast proteome). Egads! If we can’t figure this out in yeast, what hope do we have in non-model organisms?Lourdes Peña-Castillo and Timothy R. Hughes discuss this curious observation and its cause in their report in Genetics.
Frogs have been having a tough time of it lately. While there are likely many contributing factors to the global frog decline, one known cause of frog dieoff is a fungal pathogen: Batrachochytrium dendrobatidis. Unfortunately, little is known about how this aquatic fungus kills frogs or how the disease was originated and spread.
However, Dr. Jess Morgan and colleagues published in PNAS (open access article) this week a study aimed at answering the latter questions. Specifically, the authors investigated Batrachochytrium populations in the Sierra Nevada Mountains and sampled the genetic diversity. A clonal population structure with few genotypes indicates that the fungus is new to the region as it hasn’t had time to accumulate mutations. Conversely, should the disease be endemic, there should be many distinct genotypes. Without giving too much of the punchline away, the authors find evidence for an epidemic spread, though certain locations have populations that are recombining.Â Any migration of the fungus may even be human assisted.Â It will be interesting to see how the disease is controlled and the authors raise a good point here: distribution of resistant sporangia may make it easy for the organism to spread and remain dormant.Â As a result, this may be a particularly tough disease to control.
Eucalyptus is an utilitarian tree, so it’s no surprise that several organizations are interested in genetically engineering it. Indeed, its genome sequence is slated for release, which should facilitate a GE market for the species. One company in particular – ArborGen (they have a very interesting mission statement) – is using genetic engineering, cloning and classic hybridization techniques to make a cold tolerant variety. ArborGen’s grove of 355 hybrids is located in southern Alabama. While a cold tolerant genotype would enable harvest of the tree across North America, this project has been met with particular public resistance, given the species’ invasive abilities.
There may be another reason for the public to resist ArborGen’s new project: Cryptococcus gattii. Known to associate with eucalyptus, C. gattii is a yeast-like fungus that can infect and kill mammals, including humans, that inhale its spores. Recently, a rare C. gattii genotype was the subject of an outbreak in British Columbia. Scientists and environmentalists are concerned that standing groves of eucalyptus that may be inncoulated with C. gattii could result in a subsequent health hazard for anyone living nearby. This particular risk, it should be noted, is independent of genetic engineering, but rather results from increased reliance on Eucalyptus as an industrial wood (remember, it’s not native to North America). The concerned parties have raised the issue with the US Deptarment of Agriculture and the EPA, so hopefully Cryptococcus ecologists will be afforded the opportunity to determine if the pathogen lives in ArborGen’s grove.
Final note: a special thanks to Kabir Peay, a fungal ecologist, who brought this to my attention.
Take a guess: what’s the world’s largest organism? No, it’s not Yao Ming. While the Guiness Book of World Records hasn’t weighed in on this issue, scientists out of Oregon State University say that an Armillaria ostoyae individual residing in Oregon’s Blue Mountains is the largest living organism on the planet. Covering 2,200 acres, this tree killing fungus certainly is big. DNA fingerprinting and vegetative pairing confirm that a single individual spans this great distance. In addition to its great size, the fungus is quite old. By using growth rates to estimate age, this scientists estimate that this humongous fungus may be 8,000 years old.
While root rot, the tree killing phenomenon caused by A. ostoyae, slows the rate of tree harvest in a forest, the park service respects the organism’s vital role in the ecosystem. By clearing out old trees, fresh nutrients are resupplied to the soil and room is made for more resistant trees to grow. Besides, how do you kill something that is 1,600 football fields in size?
In his book Jurassic Park, Micheal Crichton imagines the possibility to extracting dinosaur DNA from mosquitos entombed in amber and using the extracts to genetically engineer T-rex and Compies alike.Â A recent discovery by an avid amber collector and scientists at Oregon State University may help enrich this park of the future: they found a 9 nine-hundredths-inch-long mushroom cap encased in a 100 million year piece of amber (yep, same age as some dinosaur fossils, conveniently enough).
To the avid mycologist out there, this should be the oldest known mushroom and will likely help our understanding of fungal evolution by providing another fossil for phylogeneticists to work with.Â Want to read more about the mushroom and the discovery of a tripartite association of the shroom with ancient insects? Check out the Oregonian, then.
I don’t know if you’ve heard, but bee colonies are disappearing! Colony collapse disorder, as this phenomenon is better known, worries bee-keepers, agriculturalists and insect admirers all over: over 25% of the commerical bee colonies have disappeared since last fall. Normally, when a commerical hive collapses, honey is left behind in the box and wild bees set up shop on top of this free resource. But it seems that wild bees are also suffering, as honey filled boxes remain bee-less.
Researchers are scrambling to determine the cause of this bee die-off. Given the agricultural implications of losing one of nature’s best pollinators, time is of the essence. All sorts of hypotheses have been suggested, from pesticides or pathogens to solar flares and cell phones, but little evidence has been accumulated (mostly due to the fact that bee bodies are rarely found).
Fortunately, a recent breakthrough occured at UCSF. Joe DiRisi’s group found, in collaboration with other researchers, that Nosema ceranae (a microsporidian) had invaded several dead bees that had been found in the wild. There are several bee pathogens in the fungi (e.g. Ascosphera apis, whose genome was recently sequenced), but the discovery of Nosema infection is notable given that Nosema apis was the cause of widespread colony collapse disorder in Spain during the mid-nineties.
So is this pathogen the cause of the widespread colony die off? The jury is still out. But this represents some of the best evidence to date that fungi may be playing a role in this unfortunate event.
Not fungal, but cool science nonetheless (plus, ants are important in some fungal symbioses). Walter R. Tschinkel uses plaster to study ant nests (particularly the Florida harvester ant, Pogonomyrmex badius) and his recent article in Bioone provides us an interesting insight into any colony morphology. Check it out.
A while back, Jason blogged briefly on a New Scientists article about the rise of a new Puccinia graminis strain, Ug99, that is spreading through West African wheat fields at an enormous rates. It looks like this story is growing in the scientific conciousness, as Science is now running an article on the spread of this wheat pandemic.
The article has a nice bit of background regarding the rise of the disease. It seems that it is spreading so quickly for due to its relatively broad host range compared to other strains. While scientists have been working to derive resistant wheat varieties, Puccinia has successfully foiled their recent attempts by mutating to acheive resistance to the plant expressed Sr24.
To boot, this strain has been found in Yemen, allowing its spores to hitch a ride along the winds that blow north along the Indian Ocean, putting much of the global bread basket at risk (I imagine that the last thing the middle east needs right now is a wheat shortage). The last time a rust spread through this area, it caused 1 billion dollars in damage. Given the extensive host range of this variety, experts predict that damages will exceede at least three times this amount.
Fortunately, researchers in Ethiopian have derived two wheat strains that may be resistant to Ug99. However, it can take several years to get these wheat strains in the ground and, ultimately, no one is certain that Ug99 won’t cleverly find a way to adapt resistance. We should keep our ears to the rail on this one: it could be a big problem.
I’ve never worked with Magnaporthe grisea, the fungus responsible for rice blast, one of the most devastating crop diseases, but I do know that its life cycle is complicated and that knocking out roughly 61% of the genes in the genome and evaluating the mutant phenotype to infer gene function is not trivial. In their recent letter to Nature, Jeon et al did what many of us have dreamed of doing in our fungus of interest: manipulate every gene to find those that contribute to a phenotype of interest.
In their study, the authors looked for pathogenecity genes. Interestingly, the defects in appressorium formation and condiation had the strongest correlation with defects pathogenicity, suggesting that these two developmental stages are crucial for virulence. Ultimately, the authors identify 203 loci involved in pathogenecity, the majority of which have no homologous hits in the sequence databases and have no clear enriched GO functions. Impressively, this constitutes the largest, unbiased list of pathogenecity genes identified for a single species (though so of us, I’m sure, may have a problem with the term “unbiased”).
If you’d like to play with their data, the authors have made it available in their ATMT Database.