Evolution of aflatoxin gene cluster

Blogging on Peer-Reviewed ResearchIgnazio Carbone and colleagues published a recent analysis of the evolution of the aflatoxin gene cluster in five Aspergillus fungi entitled “Gene duplication, modularity and adaptation in the evolution of the aflatoxin gene cluster” in BMC Evolutionary Biology. The authors were able to identify seven modules pairs of genes whose history of duplication were highly correlated. Several genomes of Aspergillus have been sequenced along with more Eurotioales fungi. Continue reading Evolution of aflatoxin gene cluster

New machines

If all went well you didn’t even notice… We migrated wiki and blog to new web server in Berkeley out of its kind hosting at OBF servers in Boston area.  We’ve started the process of rebuilding the genome browser data similar to what was deployed at fungal.genome.duke.edu server, but we are redeveloping the data dumping and importing scripts to be more automatic.  We hope this will result in a useful resource for fungal genome data including browsing and downloading annotation that is systematic and consistent across genomes.  If all goes well beyond that we’ll deploy the ideas for comparative tools across the set of genomes for the kindgom.  It will initially be to support our research interests in filamentous fungi, but we hope it will be a general enough system for other questions.

Neurospora alternative splicing

mitochondriaA quick link to a Neurospora paper in Genetics today entitled “Alternative Splicing Gives Rise to Different Isoforms of the Neurospora crassa Tob55 Protein That Vary in Their Ability to Insert ß-Barrel Proteins Into the Outer Mitochondrial Membrane”. The authors investigated alternative splicing of a gene found in the TOB complex on the outside of the mitochondria. They found reduced growth rate when a strain expressed only the the longest form of three isoforms and confirmed the protein expression of the three isoforms with mass spec.

Gene knockouts in Candida parapsilosis

Cparapsilosis from G.ButlerA recent paper “Targeted gene deletion in Candida parapsilosis demonstrates the role of secreted lipase in virulence”, from the Nosanchuk lab at Yeshiva University, shows the role of secreted lipases in virulence of this pathogen. C. parapsilosis is second only to the evolutionarily closely related commensal Candida albicans as worldwide cause of invasive candidiasis. This paper demonstrates a knockout system using selectable marker which confers resistance to the drug Nourseothricin. The authors sought to delete the adjacent and convergently-transcribed lipase genes CpLIP1 and CpLIP2 and characterize the phenotype of the lipase deficient mutants as blood-borne C. parapsilosis infections are in a lipid rich environment.

Through a series of experiments testing growth in rich media, media with olive-oil, and in infection models they showed that the importance of lipase activity. The knockout strain was unable to grow efficiently on YNB media+olive oil indicating that these two genes are the only ones capable of lipase activity. The murine infection experiments indicated that the knockout could be cleared in 4 days while the WT and reconstituted were cleared in 7. The authors acknowledge some limitations in the infection model in that it does not fully recapitulate an invasive candidiasis because mice were infected intravenously so the role of endothelial cell invasion was tested in vivo.

This is not the first paper on targeted gene knockouts in this fungus. A paper from earlier this summer, “Development of a gene knockout system in Candida parapsilosis reveals a conserved role for BCR1 in biofilm formation”, from Geraldine Butler’s group at University College group, who work on both evolutionary and pathogenesis questions in Candida species, developed a knockout system using the same drug marker. The Butler laboratory also showed that the C. parapsilosis MAT locus, part of the sexual reproduction machinery of fungi, has degraded, consistent with the observed asexuality of these species.

The improving genetic tools for targeted disruption of loci in additional species is permitting experiments that get at the heart of what makes some fungi pathogenic. With the genome sequence of many of the relatives of the pathogens we can systematically dissect what genetic differences have a role in virulence. It will be interesting to reconstruct whether the ancestor of many of these Candida spp always had the potential for virulence or if it co-evolved with its human or other mammalian commensal lifestyle.

Fusarium graminearum genome published

The genome of the wheat and cereal pathogen Fusarium graminearum was published in Science this week in an article entitled “The Fusarium graminearum Genome Reveals a Link Between Localized Polymorphism and Pathogen Specializationtion”. The project was a collaboration of many different Fusarium research groups. The genome sequencing was spearheaded by the Broad Institute at Harvard and MIT and is part of a larger project to sequence several different species of Fusarium. The group sequenced a second strain in order to identify polymorphisms.

Some of the key findings

  • The presence of Repeat Induced point-mutation (RIP) has likely limited the amount of repetitive and duplicated sequences in the genome
  • Most of the genes unique to F. graminearum (and thus not present in 4 other Fusarium spp genomes) are found in the telomeres
  • Between the sequenced strains SNP density ranged from 0 to 17.5 polymorphisms per kb.
  • Some of the genes expressed uniquely during plant infection (408 total) include known virulence factors and many plant cell-wall degrading enzymes.
  • The genes showing some of the highest SNP diversity tended to be unique to Fusarium and often unique to F. graminearum

Tracking honeybee decline

HoneybeeAn early access to article in Science A Metagenomic Survey of Microbes in Honey Bee Colony Collapse Disorder (direct link since DOI is not updated yet) using the current favorite buzzword, metagenomics, of course, describes some early work to try and discover what is killing the honeybees. It is early access and non-free and ScienceExpress is not part of our subscription here so I’ve not actually had a chance to read it yet, but the gist of the reporting about it suggest that a virus is to blame. This is in line with what Joe DeRisi and collaborators found using their Virus chip based on some news reports earlier this year, but no scientific article yet to follow this up.

Some links to today’s SFChronicle article and an article “Stung” from the New Yorker in August that alluded to this Science article.