Blogging about science

OK. It has been ages since I posted last. I just saw this article and though it was a good place to start. In the fungal pathogen world, there is a lot of debate about "what makes a pathogen" - basically, many of the human fungal pathogens out there are considered "opportunists" in that in a normal human host they are not able to cause disease. Well at least rarely are they a problem in healthy people. MFF (my fav fungus) Coccidioides is a bit more of a bear in that respect- it really does infect and kill healthy people. But a bit of an outlier.

This article reviews what is known about genomic differences between a bread mold and a pathogen. Really, there is not that much difference (and never mind that occasionally the bread mold WILL cause disease) but there are some trends that pop out. The ability to: stick to surfaces, be resistant to anti-fungal drugs, and basically be flexible- in your food source, your genetic make up and your morphology.

Another nice aspect is that the article is open source! Devour at will!

Eurotiomycetes are my favorite

In 1997 Ericksson and Winka described the class Eurotiomycetes when new ordinal descriptions of the Ascomycota were completed. At the time, only a single order, Eurotiales, was assigned to the class. Over the last ten years, a more complete picture has developed, such that the most recent analysis shows that the class contains at least two subclasses, Eurotiomycetidae and Chaetothyriomycetidae, based on a five gene Bayesian tree (Geiser et al. 2006).
The number of orders contained in the class has also increased. The Eurotiales is still a well-supported order, now placed within the subclass Eurotiomycetidae. In addition, the Onygenales, a previously recognized order in the Plectomycetes (the previous class name) containing many vertebrate pathogens, is a member of the Eurotiomycetidae (Kuraishi et al. 2000). There are an additional 3 orders that will likely be placed in that subclass, the Ascosphearales, Aracnomycetales, and Coryneliales (Gibas et al. 2002, Geiser et al. 2006). The other subclass, Chaetothyriomycetidae, contains three well-supported orders, Chaetothyriales, Verrucariales and Pyrenulales (Tree of Life 2007, Haase et al. 1995). The last order contained in the Eurotiomycetes, the Mycocaliciales, may be a subclass, as it appears to be a sister taxon to the Eurotiomycetidae and Chaetothyriomycetidae, but that observation is based on too few data at this time and thus it is still included within the Chaetothyriomycetidae (Geiser et al. 2006).
The ancestral state of Ascomycota is uncertain and debated (James et al. 2006). The subphylum Taphrinomycotina is the most likely basal group of the Ascomycota (Liu and Hall 2004). This group is highly variable in lifestyle, form and biochemistry. Thus, the ancestral state for the subphylum Pezizomycotina, the group that contains the Eurotiomycetes, is unclear. It has been stated that lichen containing groups must be derived from lichenized ancestors, due to lower rates of gain of lichenized habit than loss (Lutzoni 2001). From that statement, the ancestor to Pezizomycotina must be a lichenized fungus, as this group contains the lineages leading to lichenized fungi. However, due to the high degree of variation in the taxa of the photobionts, and the form and distribution of the lichenized fungi within the group, one could argue that convergent evolution could also explain the pattern observed.
The field of fungal phylogenetics is in the early stages of clarifying relationships among groups. In addition, sampling of these various groups is incomplete. However, recent work on the Eurotiomycete lineage is developing a clearer picture of the organization within that group (Geiser et al. 2006, James et al. 2006). Within the framework of these analyses, patterns of lifestyle can now be added into the analysis to develop hypotheses regarding the likely ancestral state of the Eurotiomycetes.

Plans for next month

All in all a good meeting. My talk went well, of course didn't say everything I wanted, in exactly the way I wanted, but I think it was OK. The main points got across. First Gordon conference, and I think I'll try to go next time around, in 2 years, provided I am still in mycology. John Taylor will be a co-chair, so bound to be lots of things I am interested in.

So, this week here in Tucson, getting caught up on some papers, and hopefully getting some work done around the house. Then off to Billings for a week. Really looking forward to it! Will be great to see family, and we're also planning a backpacking trip in the Beartooths.

Then home again for a week, and off to the ESA meeting in Milwaukee. Mainly going for the Fungal ecology workshop, as I got a scholarship to attend the meeting from FESIN.

good summer!

Meeting time

I'll be heading to a Gordon Conference next week. Specifically, the Cellular & molecular fungal biology conference. I have to give a talk, so will be occupied with that, and not so much blogging. But I'll try to summarize some of the cool work if I can.

Yeast are smarter than people

A recent post on a great site, Panda's Thumb, summarizes a recent article on de novo origination of a gene. What does this mean? de novo is latin for "from new", and its usage is wide, and can mean different things. It can mean "newly arisen function," and might also be referred to as ab initio, or "from the beginning." Anyway, the paper basically shows how brewer's yeast made a brand new gene from a set of nucleotides.

Host resistence to fungal pathogens

The basis of mammalian host resistance to fungal pathogens is relatively under studied. But what is the best model system for studying fungal disease? Many fungi are not host specific, that is, they have the ability to be virulent in many different hosts. Experiments can not be done in vivo in humans, but can they be done on human cell lines. Is a mouse model appropriate for understanding general mammalian immunity? Because mouse studies can be extremely expensive and a regulatory time suck, perhaps other models may be appropriate for understanding virulence in fungi (Casadevall 2005).
Recent work with C. neoformans shows that interactions with other soil organisms can be informative in screening virulence factors (Mylonakis et al. 2002). Further work in this system has revealed a specific gene required for pathogenicity in mice (Tang, et al. 2005). Other systems such as Aspergillus flavus and Candida albicans with the wax moth have also been described and show promise (Brennan et al. 2002; St. Leger et al. 2000). Another tool that is also being used to identify virulence factors in fungi is genome sequencing. Currently, several fungi are sequenced, or in the pipeline. Annotation has proven more difficult than originally thought, so the completeness of the data is limited as of now, and makes searching for "pathogenicity genes" using bioinformatic tools complicated and cumbersome.
The basis of host immunity to fungi is understood at a certain level. When mice without CD4+ lymphocytes are vaccinated with an attenuated Blastomyces dermatitidis and Histoplasma capsulatum vaccine, CD8+ T cells can induce and maintain protective immunity (Wüthrich et al. 2003). Vaccine mediated protection was accompanied by reduced inflammation and fungal burden in the lung. In experiments with mice lacking both CD4+ and CD8+ T lymphocytes, the mice were not able to control the fungal burden very effectively with vaccination, but did show some resistance. Hence, the possibility that antibodies and/or B cells, in addition to other cell types, such as dendritic or NK cells, may play a role in the development of antifungal immunity, and has implications for vaccine development. The main result of this study is that even in the absence of CD4+ T cells, such as in AIDS patients, some immunity to fungal infections was obtained.

the PZ effect

Ha! funny. Never would I get a hit, but because PZ linked my blog, I got 2 comments. 1 nice person, and 1 crazy person.

If ppl want to read about my bits, fits and starts, be my guest. Say hi once in a while, and plz let me know if I say something factually inaccurate.

I love keeping my toes in restoration ecology, because I think that is what hooked me into biology. That and my 7th grade biology teacher who taught me my first Punnett's square. I love genomics, the fusion of computer sciences and biology. I also think the future is in the soil. I used to be a plant ecology/ plant genetics person. But once I got out in the field, I realized the soil is the great unknown in plant ecology.

Now I study fungi. Soil fungi. Ascomycota, generally. Eurotiomycetes, specifically. Well, even more so, Onygenales. And for my PhD primarily Coccidioides. And know you know all there is to know.