I already mentioned (here and here) the New Phytologist Symposium on Bioenergy Trees, but I’d like to let you know that my meeting commentary has been published in the journal. I highly recommend attending one of the many New Phytologist Symposia based on their intimate size and the excellent quality of speakers.
A paper published in the recent issue of PNAS “Insights into the oxidative degradation of cellulose by a copper metalloenzyme that exploits biomass components” by Quinlan et al. succeeds in characterizing an important aspect of the breakdown of cellulose by enzymes. I’m interested in the use of cellulose in bioenergy purposes, but one of the major problems in its use is extreme recalcitrance of the polysaccaride. By fully understanding the enzymatic mechanisms of the breakdown of cellulose we can surpass a major scientific and economic challenge for the effective release of bioenergy from biomass.
Cellulose is typically broken down by fungi employing a suite of different enzymes. These enzymes are traditionally placed into two classes: endoglucanases and cellobiohydrolases. In this paper, the authors identify the enzymatic abilities of a newly recognized enzyme class, called the GH61 glycoside hydrolases (see Harris et al. for more information on GH61 glycoside hydrolases). The GH61 glycoside hydrolases greatly increase the efficiency of the endoglucanases and cellobiohydrolases and recent genome sequencing of brown rot fungi, such as Postia placenta, show numerous GH61 glycoside hydrolases.
The authors describe the 3D structure of a GH61 glycoside hydrolase from Thermoascus aurantiacus identifying the active site details and catalytic activity of the enzyme. It was identified that the GH61 glycoside hydrolase enzymes are oxidizing agents and the authors show the direct degradation of cellulose. Furthermore, the authors identify copper as the metal cofactor of the enzyme and show a unique methyl modification of a metal-coordinating histidine residue.
See here for commentary on the paper.
In yesterday’s New York Times is a nice opinion piece from Ian Lipkin on real life and real life infectious outbreaks. You should read it.
Here’s an interesting short film on the “viral” marketing of the movie Contagion. Obviously, it’s not viral, but bacterial and fungal marketing.
I haven’t seen the movie, so I can’t endorse it one way or another, but I will say Steven Soderburgh has a pretty great track record when it comes to movies. The above video shows a fascinating way to advertise this movie to audiences (See Jonathan Eisen’s blog post on the subject here).
I found the Li et al. paper – “Structural Variation in Two Human Genomes Mapped by Whole Genome de novo Assembly” – published in the August issue of Nature Biotechnology interesting for a number of reasons. As someone mainly interested in fungal and plant genomics this paper is somewhat outside my research focus, but I found both the novel approach to de novo genome assembly and the emphasis on structural genome variation over single nucleotide polymorphisms (SNPs) in explaining genetic diversity to be very interesting.
By using short read sequencing technology from the Illumina platform, the researchers began by sequencing the genomes of two individuals, one person of African descent (NA18507) and one of Asian descent (YH). As with many genome sequencing studies, there were numerous problems during the assembly process, such as alignment accuracy, recovery of long contiguous stretches of nucleotides, stretches of low or no coverage, and identifying sequencing background noise. The authors tried to eliminate these issues by developing a strategy focusing on de novo assembly instead of mapping reads to reference genomes.
The novel pipeline was able to identify structural variants – such as insertions, deletions, rearrangements, inversions, etc. – in each of the homozygous assembled genomes, some of which were upwards of 23,000 base pairs in length. The researchers then validated the structural variations using both experimental and computational methods, and, using data generated for the 1000 Human Genomes Project, they mapped their identified structural variations in the genomes of 106 other individuals.
While SNPs are easier to observe (perhaps the reasons why they have been emphasized so much in recent years?) it seems that structural rearrangements are perhaps the major form of variation in human genomes, and maybe, all genomes. Structural variations were less common than SNPs, but are more individual specific and appear to be associated with phenotypic characteristics. A next research direction would be to observe the association of structural variations to disease traits or susceptibility.
This paper also suggests that accurately assembling long genomic regions are very important to understanding structural variation. This can be accomplished by either using technologies that naturally generate longer reads (i.e. Sanger or PacBio sequencing) or ensuring that short reads can be accurately assembled by computational methods.