Genetics of Late Blight Fungus Discussion Group

Potato Late Blight On-line Workshop
The Fungus and the Disease
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Genetics of the Fungus

A lot of headway has been made in understanding the genetics of P. infestans, and in developing techniques for the classical and molecular genetic analysis of the organism in the laboratory. But we are still in the early stages of exploiting those abilities.

What do we need to know about the genetics of P. infestans? Do we understand enough about the natural genetic cycles of the organism? Do we know enough about its genome, and just how much variability exists between different isolates? What can we do in the laboratory to identify genes that are important to the biology and pathology of the organism?

At the late blight meeting in Tucson, several areas for future research were suggested:

1. Identify genotypic diversity in P. infestans populations nationwide, so that scientists and growers know as much as possible about the populations they are dealing with. This may require the development of improved genetic markers for P. infestans.

2. Evaluate the role of recombination in generating new types of P. infestans, to indicate the likelihood of new variants developing and guide studies of epidemiology.

3. Expand our understanding of the genetics of host-pathogen interactions, to understand host specificity, virulence, and aggressiveness in P. infestans.

4. Drastically increase efforts to advance the basic genetics (and biology!) of the P. Infestans system to allow us to make inroads in the above subject areas.

What else do we need to do and what are the highest priorities?

Howard Judelson - 05:29pm Feb 20, 1997
A lot of the research in P. infestans is going to be genome-based, and to assist this process genetic maps, libraries and other tools are being developed in several labs. But this raises an important question: how much variability is there going to be between isolates? The sexual cycle is not very frequent in P. infestans, so there has not been much selection for conservation of genome structure, gene order, etc. Does anyone have any insight into this potential problem?

Steve Goodwin - 06:24pm Feb 20, 1997
Although the sexual cycle is infrequent outside Mexico, within Mexico it probably occurs every year. Therefore, isolates from sexually reproducing populations in central Mexico may have a more uniform genome organization - using isolates from outside Mexico is asking for trouble. We know that aneuploidy, at least for the chromosome containing the Gpi locus, occurs commonly even in field isolates (e.g., US-8 and US-11), so I think it will be necessary to screen even isolates from central Mexico for aneuploidy. But I don't know of an easy way to do that, except with a battery of highly polymorphic co-dominant markers.

Thomas Randall - 04:12pm Feb 27, 1997
Metalaxyl resistance seems to have spread around the world quite rapidly, since a high frequency of isolates in different regions throughout the world are resistant. Does anybody have an idea of how this resistance is being spread or how often resistance can spontateously develop. Is the same locus responsible for different populations of resistant P. infestans or are there a variety of loci which can cause resistance? Along the same lines, has anyone done much on how new isolates of P. infestans get distributed and established at different places.

Didier Andrivon - 12:59am Mar 5, 1997
Thomas,
I know of very little work dealing with the genetics of metalaxyl resistance, except that of Richard Shattock (he found resistance to be monogenic, if I recall correctly). It's difficult to get really positive about resistance genetics in P. infestans, for at least two reasons: first, genetic analysis in P. infestans is not really straightforward, due to the low germination rate of oospores which might bias the ratios in progeny testing; second, as far as I'm aware, the work on metalaxyl resistance genetics was done with isolates that were either sensitive or highly resistant to the chemical. Right now, we see a great deal of sensitivity levels in current populations, which might mean a polygenic inheritance for resistance. Since resistance arose very rapidly after the chemical was released for commercial use, and can be found in many different lineages (including 'old' ones) I would tend to think that variation (or at least potential variation) for metalaxyl resistance is no problem at all for the fungus to develop.

Jean Ristaino - 11:01am Mar 27, 1997
We (Fraser, Shoemaker and Ristaino) have observed variation in sensitivity to metalaxyl in populations of P. infestans in North Carolina tomato fields. Isolates are not either resistant or sensitive but exhibit a range of variation in sensitivity to the fungicide. We have also found a few isolates that were US-7 and US-8 by allozyme genotyping that were sensitive to metalaxyl. This means that allozyme genotype alone can not be used as a measure of sensitivity unless you are dealing with US-1 which always appears sensitive to the fungicide.

Didier Andrivon - 01:20am Mar 28, 1997
Jean,
I totally agree with you on the point that allozyme genotypes are not saying much about metalaxyl sensitivity, and I would extend this remark to US-1 as well as to the newer genotypes. We tested here some isolates collected in South Africa by Freddie Denner, and all showed allozymes typical of US-1. These isolates showed all the different metalaxyl sensitivities we're able to detect with our leaf disk test. I don't think there is any good reason why US-1 could not evolve metalaxyl resistance if selection for it is present.

Howard Judelson - 08:14pm Apr 1, 1997
Dear Phytophthorologists:
There is lots of concern about having the A1 and A2 types together in the same region, since that could lead to recombination and the development of new genotypes. But how about the parasexual cycle? There are a few studies, mostly from the 60s and 70s, that suggest that some form of somatic fusion can take place between isolates of the same mating type. Are there any newer data that indicates how common somatic fusion is?