Title: Genome Evolution in the Irish Potato Famine Pathogen Lineage
We face a crisis in food production and food prices. (New York Times article from Feb 4th) If you can’t eat, you don’t worry about cancer.
World population is expected to peak at 9billion, and we’re not producing enough food. One aspect of that is crop diseases, which could allow millions more to be fed if we could overcome this problem.
One of the most important is oomycete Phytophthora – (latin: plant destroyer), kills dicots – 10’s of Billions of dollars worth annually. World’s biggest potato producer is China.
P.infestans suppresses or triggers plant immunity. Able to invade cells, and forms stuctures between cells. (hyphae)
Some plants carry resistance and have an apoptosis like response. Resistant plants also suppress the immunity supressors. [strange phrasing is all mine.]
Genome sequence of Phytophthora infestans is complete. Published last year. (Cover of nature – a rotten potato!)
Compare P infestans genome to others of the family – very large expansion. Number of genes is about the same, but 240Mbp vs. 65-95Mbp. Much of it is repeat driven.
Effectors (immunity suppressors) typically occur in expanded repeat-rich and gene-poor loci. (Examples :RXLR, AVR4)
Most of the genes in the genome are all clustered with 1kb of each other, except for a spattering that occur in the repeat-rich regions. This is an unusual distribution.
Core othologs are all in the clustered regular regions, effector genes all seem to be in the repeat-rich, again, unusual distribution.
Some discussion of how the parasite evolved along with “host jumping”. Resequenced several isolates of 4 related strains. (all of which have the large genome expansion), and compared them.
4-fold number of genes missing in repeat region vs non-repeat regions. Repeat regions are more plastic. Look at dn/ds, and there is also different selection pressures between the two.
Repeat regions are also highly enriched in genes induced during colonization of tomato and potato (Raffaele et al, Science 2010)
- Core genome- high density region/low repeat content
- “plastic” region – low gene density/high repeat content
- high rates of gene turnover and positive selection in the plastic genome
- “niches” in the genome for rapid effector evolution.
- Unexpected rapidly-evolving “plastic” genome familes – cell wall hydrolases, histone and rRNA methyltransferases. [wasn’t discussed in the talk, as far as I can tell, bt interesting nonetheless.]
Using Genomics to improve isease resistance. Emergence of P infestans “blue 13” clone which is dominating UK isolates, but was barely present 10 years ago.
Core effectors as targets for resistance.
Synthetic R genes with expanded effector recognition. (modify potato genes to improve resistance.) Expansion: An R3a mutatnt that recognizes both AVR3a(ki and em form), it is expected to be effective against all P.infestans isolates. Did create this in the lab… and some success. some clones were able to trigger cell death response.
Single resitue mutations expand effector recognition.
Non-Gm solution through genome editing?
The knowledge of pathogen effectors and comparative genomes is essential.
[Again, a neat talk on a topic I knew nothing about. Well delivered and very clearly explained.]