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.
CNN reports on a giant (25 ft tall) prehistoric fungus classified by C. Kevin Boyce and collegues. Also see U Chicago press release and Softpedia articles about the manuscript entitled Devonian landscape heterogeneity recorded by a giant fungus published in Geology describing the Prototaxites fossil.Â It has apparently been studied for quite a long time (150 years) to no avail as to whether it was fungus, algae, or lichen prior to this study.
We got word last week from the JGI that our DNA for Neurospora tetrasperma and N. discreta have passed QC and library QC and are on their way to being sequenced. The center also plans to do some EST sequencing to improve gene calling abilities.
Why more Neurospora genomes? The sequencing proposal discussed these species as a model system for evolutionary and ecological genetics. It will allow us and others to test several hypotheses about the molecular evolution of things like genome defense in Neurospora and to understand more about the evolutionary history of the model organism N. crassa.
Continue reading More Neurospora genomes
We have also posted our presentations from Fungal Genetics 2007 on our site as well including John’s talk and mine.
Continue reading Presentations on slideshare
A paper in PLoS One, Assessing Performance of Orthology Detection Strategies Applied to Eukaryotic Genomes, reports a new approach to assess the performance of automated orthology detection. These authors also wrote the OrthoMCL (2006 DB paper, 2003 algorithm paper) which uses MCL to build orthologous gene families. The authors discuss the trade-offs between highly
sensitive specific tree-based methods and fast but less sensitive approaches of the Best-Reciprocal-Hits from BLAST or FASTA or some of the hybrid approaches. The authors employ Latent Class Analysis (LCA) to aid in “evaluation and optimization of a comprehensive set of orthology detection methods, providing a guide for selecting methods and appropriate parameters”. LCA is also the statistical basis for feature choice in combing gene predictions into a single set of gene calls in GLEAN written by many of the same authors including Aaron Mackey.
I’ve been reading a lot of orthology and gene tree-species tree reconcilation papers lately, some are listed in Ian Holmes’s group as well as listing some of the software on the BioPerl site. This also follows with on our Phyloinformatics hackathon work which we are trying to formalize in some more documentation for phyloinformatics pipelines to support some of the described use cases. I’m also applying some of this to a tutorial I’m teaching at ISMB2007 this summer.
The New Scientist has an article about the spread of black stem rust caused by Puccinia graminis. We briefly mentioned the 1st release of a Puccinia genome in January. Some more links about the spread of the Ug99 virulent strain.
Continue reading Puccinia black stem rust disease spreading
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.
Perhaps not a surprise to anyone that has dabbled in evolutionary analysis of proteins, Kawahara and Imanishi (BMC Evolutionary Biology 2007) confirm that not every protein evolves via a molecular clock in Saccharomyces sensu scricto. Using everyone’s favorite evolutionary tool, PAML, the authors identify protein lineages via a whole genome scan that evolve relatively slow or fast compared to the rest of the clade. Some changes even appear to be due to the invisible hand of natural selection and independent of the complications that may have arisen during the whole genome duplication in the ancestor of this clade.
It has been previously speculated that, either upon protein duplication or change in the selective regime of the environment, a protein may rapidly evolve at speciation and then, upon obtaining a new, important function, slow down it’s evolutionary rate to a clock-like tempo. One of the black boxes in this hypothesis is whether or not closely related proteins can rapidly diverge. While the authors are not able to identify a mechanism explaining how, their study demonstrates the plausibility of this hypothesis. However, it remains uncertain if proteins that exhibit rapid divergence will subsequently slow down their evolutionary rate later in time.
It’s good to see evolutionary analysis being applied to fungal genomes. With so many sequenced species spanning a great range of phylogenetic distance, the fungal kingdom is poised to provide great insight into the evolution of eukaryotes.