Eukaryotic Microbiology: Two Weeks In

Have the second week of Eukaryotic Microbiology in the books (except for some residual grading to complete). So far we've covered Candida albicans and two Fusarium spp. Last week was C. albicans and we discussed two papers. (I'm not including the review articles students read at the beginning of each week.):

• An isochromosome confers drug resistance in vivo by amplification of two genes, ERG11 and TAC1. Selmecki A, Gerami-Nejad M, Paulson C, Forche A, Berman J. Mol Microbiol. 2008 May;68(3):624-41
• Self-regulation of Candida albicans population size during GI colonization.
• White SJ, Rosenbach A, Lephart P, Nguyen D, Benjamin A, Tzipori S, Whiteway M, Mecsas J, Kumamoto CA. PLoS Pathog. 2007 Dec;3(12):e184

And this week was Fusarium and we discussed:

• Comparative genomics reveals mobile pathogenicity chromosomes in Fusarium. Ma LJ, van der Does HC, Borkovich KA, Coleman JJ, Daboussi MJ, Di Pietro A, Dufresne M,... Cuomo CA, Kistler HC, Rep M. Nature. 2010 Mar 18;464(7287):367-73. doi:10.1038/nature08850
• Two Cdc2 Kinase Genes with Distinct Functions in Vegetative and Infectious Hyphae in Fusarium graminearum. Liu H, Zhang S, Ma J, Dai Y, Li C, Lyu X, Wang C, Xu JR. PLoS Pathog. 2015 Jun 17;11(6):e1004913. doi: 10.1371/journal.ppat.1004913

While I planned to discuss each week individually, these end up going well together, plus this is a difficult time of the semester for me guaranteeing I can't write as frequently as I would like.

So we stay within the ascomycota for the first two weeks. Some things that I wanted to emphasize in class and that came from the students:

• What does it mean to be 'wild-type'? This came up with regards to a 'wild-type' genomic sequence. Is the CFTR mutation (the allele that causes cystic fibrosis when homozygous) a mutant genotype? Does the fact that in the caucasian population a cystic fibrosis causing mutation in the CFTR gene occurs with a frequency of 0.025 make a difference? What about the allele that causes sickle cell anemia when homozygous? People who have a 'mutant' allele and a 'normal' allele are more resistant to malaria, so this mutation is potentially beneficial.
• How is phenotypic diversity generated in asexual organisms? This is an important question because sexual reproduction is promotes phenotypic diversity in many eukaryotes. However, there are significant issues associated with sexual reproduction that prevents using it as a simple explanation for phenotypic diversity.
• How do organisms adapt to their environment and is a pathogen really any different from any other organism (short answer is 'no')?
• How do duplicated genes evolve? This (Lui paper) goes hand-in-hand with the Candida Selmecki et al paper and the Fusarium Ma paper.

We'll be revisiting many of these issues throughout the semester. We spend a fair amount of time dealing with specific aspects of the papers, but I try to highlight some of these broader issues. This week we tackle Cryptococcus neoformans and will highlight at least one of the above issues again.