Dr Celeste Linde Lecturer Phone: 61 2 6125 7682 Fax: 61 2 6125 5573 celeste.linde@anu.edu.au

Main Research Interest
Population genetics, evolution, phylogeography and molecular phylogenetics of plant pathogens.

Background
Born and bred in South Africa, also received my formal education there. I started off in forest pathology under the guidance of Mike Wingfield. My main focus was on the Oomycetes (Pythium and Phytophthora), although one could not avoid to appreciate the complexities of other forest pathogens as well. I eventually obtained a PhD on the population genetic structure of Phytophthora cinnamomi . During my PhD, André Drenth (Australia, Brisbane) invited me to spend six months in his lab, making sure that I at least get some population genetics in my head, and that I will always think back fondly of Australia.   Now I do not need to think back... I am back in Ozzie land!   After my PhD I spend some time at the Agricultural Research Council (Infruitec, South Africa) on root and crown rot diseases of fruit trees. I then switched to cereal diseases and more specifically, their population genetic structures, at the ETH Zürich, Switzerland, with Bruce McDonald. Neither Bruce nor I was really sure how long I would/could stay, but in the end I spend five wonderful years there. During this time, I met many wonderful people, cycled up many mountains, and also entered the world of Rhynchosporium secalis, a fungal leaf pathogen of barley.

Research
My current research will continue on the population genetics of Rhynchosporium secalis , barley scald pathogen. Barley is a crop that is extensively grown in many countries, including Australia, and crop losses due to scald can be high (30-60% crop losses have been reported). The host, barley, originally is from the Fertile Crescent (Middle East), with a secondary centre of diversity in Ethiopia (northern Africa). It is commonly assumed that barley and R. secalis co-evolved. However, many hosts other than cultivated barley (Hordeum vulgare) are also susceptible to scald. Some questions we are addressing include: 1. Did barley and R. secalis co-evolve (centre of origin?), 2. Do other hosts act as an inoculum reservoir for cultivated barley, 3. How many Rhynchosporium species are involved, and 4. How did R. secalis spread around the world (gene flow). These questions can be answered with many techniques, of which RFLPs has been used in the past, but we will concentrate on sequence and microsatellite analyses in the future. This work is under well underway in a PhD project of Pascal Zaffarano and my own research. Our recent development of microsatellite markers for R. secalis is particularly exciting as it opens up a few possibilities to do mark-release-recapture experiments. One such project is looking at the relative contribution of sexual and asexual spores to the epidemic in Syria (project lead by Mathew Abang).

Rhynchosporium secalis has long been considered as a fungus that can reproduce only asexually. However, our work now show quite convincingly that the fungus must undergo at least some sexual reproduction cycles to account for high levels of genetic diversity, frequency dependent mating-type selection, and recombination within sequencing loci. Identifying the mating-type loci now also permits us to make controlled crosses. Unfortunately, we still have not been able to initiate the production of sexual fruiting bodies!

I am also interested in the evolution of virulence in R. secalis. Host resistance in barley does not last very long, especially if it is resistance governed by a major gene. This means the pathogen is able to evolve virulence fairly quickly. Stéphanie Schürch examined the mechanisms that R. secalis use to overcome host resistance, and found deletion of the avirulence gene very common. Question now is, how does virulence evolve on different hosts?

On a general tone, I try to figure out what make pathogens evolve and which of the evolutionary forces plays the most important role. Pathogen populations evolve in response to the control measures deployed against them, with some pathogens evolving to counteract the control measures more rapidly than others.   In plant agricultural ecosystems, the most common control measures are the deployment of resistance genes and the application of pesticides (mainly fungicides). Bruce and I developed a risk assessment model and tested it against empirical data to assess the relative impact of migration, reproduction system, and population size on the evolutionary potential of pathogens in plant agroecosystems. The predictive power of our risk model was compared against an existing risk model for fungicide resistance.   The new model predicted the emergence of fungicide resistance better than the existing model and indicated that migration rather than fungicide class was the most important factor driving pathogen evolution in agroecosystems. The significance of migration was similar across different selection pressures (host plant resistance, pesticides) and pathogenic agents (fungi, nematodes, viruses), suggesting that these findings may be applicable to a wide range of pathogens across biological systems. These findings were particularly important because: 1. Pathogens are important components of all ecosystems and affect all human societies either directly (eg sick people, crops, and animals) or indirectly (eg higher food costs and contaminated food supplies, burden on health-care systems).   2.   Pathogen evolution is well-recognized as a major problem in agriculture and medicine [eg antibiotic and fungicide resistance, host jumps (SARS recently, numerous other viruses such as HIV and fungal plant pathogens in the past), overcoming plant resistance genes and evasion of mammalian immune systems].   3. Internationalization of travel and trade is likely to increase rather than decrease, and our findings suggest that public health organizations, including APHIS, may be able to use the ranking of pathogen evolutionary potential to better prioritize pathogens for quarantine purposes.  

Current Students

• Pascal Zaffarano (PhD candidate, ETH Zürich) 2003-onward.
• Stefano Torriani (Diploma student, ETH Zürich) 2004.

Current Funding

• ETH Research Grant- Switzerland (2003-2006) (178,000 CHF). Population genetics and phylogeography of the scald pathogen Rhynchosporium secalis.

Publications 2004-08 (Full publication list)
Barrett, L.G., Thrall, P.H., Burdon, J.J., Nicotra, A.B., Linde, C.C. 2008. Population structure and diversity in sexual and asexual populations of the pathogenic fungus Melampsora lini. Molecular Ecology 17: 3401-3415.

Groenewald, M., Linde, C.C., Groenewald, J.Z., Crous, P.W. 2008. Indirect evidence for sexual reproduction in Cercospora beticola populations from sugar beet. Plant Pathology 57: 25-32.

Zaffarano, P.L., McDonald, B.A., Linde, C.C. 2008. Rapid speciation following recent host shifts in the plant pathogenic fungus Rhynchosporium. Evolution 61(6): 1418-1436.

Groenewald, M., Groenewald, J.Z., Linde, C.C., Crous, P.W. 2007. Development of polymorphic microsatellite and single nucleotide polymorphism markers for Cercospora beticola (Mycosphaerellaceae). Molecular Ecology Notes 7: 890-892.

Koopman, T., Linde, C.C., Fourie, P.H., McLeod, A. 2007. Population genetic structure of Plasmopara viticola in the Western Cape Province of South Africa. Molecular Plant Pathology 8(6): 723-736.

Gobbin, D., Rumbou, A., Linde, C.C., Gessler, C. 2006. Population genetic structure of Plasmopara viticola after 125 years of colonization in European vineyards. Molecular Plant Pathology 7(6): 519-531.

Linde, C., Zala, M., McDonald, B., (2005) “Isolation and characterization of microsatellite loci from the barley scald pathogen, Rhynchosporium secalis”, Molecular Ecology Notes (electronic), Vol 5, pp 546-548.

Linde, C., Zala, M., Paulraj, R., McDonald, B., Gnanamanickam, S., (2005) “Population structure of the rice sheath blight pathogen Rhizoctonia solani AG-1 IA from India”, European Journal of Plant Pathology, Vol 112, pp 113-121.

Schürch, S., Linde, C. C., Knogge, W., Jackson, L. F., and McDonald, B. A. 2004. Molecular population genetic analysis differentiates two virulence mechanisms of the fungal avirulence gene NIP1 . Molecular Plant Microbe Interactions in press.

Teaching
I teach the following course starting 1 st semester 2005.

Microbial-Plant-Pathogen Interactions: BIOL3102
This is a third year course in which we will explore the diverse roles of micro-organisms, especially fungi, in the life cycles of plants. Topics will include the identification, epidemiology, pathology, biocontrol with eg. induced host resistance, host interactions (gene for gene interactions and quantitative resistance), and the evolution and population biology of plant microbes and plant pathogens. Lecturers should include active researchers from CSIRO and RSBS.

Possible Honours Projects
I am open for discussion.