Dr Gretna Weste (1917-2006), botanist

Dr Gretna Weste. Interview sponsored by the Australian Government as an ongoing project from the 1999 International Year of Older Persons.

Gretna Margaret Weste was born in 1917 in Dumfries, Scotland. She completed a BSc (1938), MSc (1939) and PhD (1968) at the University of Melbourne. Dr Weste became a leading Australian plant pathologist, with expertise in jarrah dieback. Dr Weste published over 100 research papers and provided advice to national and regional parks with dieback problems. She was Senior Associate in the School of Botany at the University of Melbourne and, after her retirement, continued to work there on a voluntary basis supervising postgraduate research students and lecturing to final year undergraduate students. Dr Weste passed away in 2006.

Interviewed by Professor Nancy Millis in 2000.


Inspired to be a botanist

I have the great pleasure of talking with Principal Fellow, Associate Professor Gretna Weste, of the Botany School at the University of Melbourne – a very old friend. Gretna, as one Aussie to another: were you actually born in Australia?

No, I was born in Scotland, although my parents were Australian. My father, who had an MSc in chemistry and a postgraduate diploma, was a volunteer chemist in World War I. He went over and did a month in various labs, including one at Cambridge with Lord Rutherford, and then went up to Gretna, a town about 20 miles from Gretna Green. Hence my name: I was born at a munitions factory where they were making explosives for the war – not a bit romantic! I turned two on the boat in which we came back to Australia after the war.

I think you lived in a fairly open part of Melbourne, with not many neighbours.

We had a huge, very old timber house in Surrey Hills, with several levels, and four blocks of land, most of which was wild. My young brother and I played cowboys and Indians and all that sort of thing. We didn’t really know our neighbours.

My parents were very keen on camping, and would hire a greengrocer’s van and horse and take off to the hills for three weeks. When I was still only five and my brother was four, we went down to Wilsons Promontory. You had to catch the train to Foster and then drive in a jinker out along the beach. We camped at Darby River (the river was too deep for us; we were dipped in) and moved on to Tidal River. We walked across to Sealers Cove, each carrying a blanket on our backs, and camped the night. I don’t remember any track, but I remember very clearly the place where we slept. It was good fun.

My mother was a country lass who became a nurse. She was very interested in the bush and in plants, and that’s probably what inspired me. When I was eight we went up Mount Buller – my brother and I each carrying our blanket again, and my parents carrying my baby sister up – and the flowers there were so beautiful that I decided then and there to be a botanist. And I’ve never changed.

Did your school encourage you to include science among your interests?

At Mont Albert State School I was chiefly distinguished because I was bigger and older than the others – I got through the work and talked, which got me into trouble. And I got the strap for not being able to draw. After a couple of years there, I went to a small private school and studied ordinary subjects, with no science. When that school closed, I got a scholarship to Methodist Ladies’ College – but I still didn’t do science: by then the Depression was upon us and I had to get a scholarship. I got a senior government scholarship, a Queen’s scholarship and an Exhibition in botany. I should say I was keen on sport. I was mad on playing basketball (now called netball) and I was in the team.

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Why is reaction wood different?

At the time you went to university, not many people – particularly not women – were given a good grounding in basic science. How did you take botany, your first love, into a science degree?

Well, I matriculated in arts subjects – English literature, French, history and so on, with some botany and biology. When I went up to the university, with my scholarship and my Exhibition to keep me, I had to pick up physics, chemistry and maths. I enjoyed them, particularly the physics, and I did quite well in the first year. (When later I was on the staff, I always acted to keep the opportunities open, not to set rigid prerequisites. Plenty of people are bright enough to have the ability to pick things up, and why shouldn’t they have that chance?)

I was interested in chemistry as well as botany – how things worked, rather than taxonomy. I did zoology in second year, but as an extra subject I did chemistry and then agricultural chemistry, which is such a good adjunct to botany and which I thoroughly enjoyed. Our lecturer in that, Mr (later Professor) Leeper, was wonderful, the best lecturer I ever had. I graduated with first class honours, exhibitions and a Howitt natural history scholarship, and then I went on to do an MSc in reaction wood.

What on earth is reaction wood? Does it mean your axe is too blunt?

No. I worked at CSIRO Forest Products, which had found in cutting timber that the wood from a curved side of a branch behaved completely differently from wood that was straight up and down. In softwoods it is called compression wood and it is well known to occur on the inner side, but my MSc was the first work on hardwoods.

In all my research I’ve worked on a question-and-answer principle. I took as my problem: Why is this wood different? Why is it behaving so differently? I cut down all the curved tops of trees that I could find. My father had some land up at Olinda, so I had the trees there cut down; I got Nothofagus and blackwoods everywhere I went, and I got some logs sent to me from the Forestry and Timber Bureau in Canberra. We found out that the wood had a completely different structure. It had an inner lining and was extremely tough – it had to stand the strain of bearing the heavy crown on a bent, curved axis, instead of having it supported by the roots up and down. That was quite interesting and quite important.

I did that work in 1938, taking out my MSc in 1939. In those days you couldn’t do a PhD in Melbourne; you had to go overseas. But that was not a time to go overseas, because war was imminent.

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Woman’s place: a science masquerade, and family priorities

What came then?

I got a job as a research officer in the Forest Commission. They were very worried about all their pulpwood, which had been killed (but not burnt) in some terrific fires in 1939. Mountain ash is highly susceptible to decay, so how were they going to preserve it? We did experiments to find out what was decaying and how we could prevent further damage.

Shortly after I got there, however – appointed with a letter as a research officer – I was told I was a temporary typist. That was the only rate for a woman, unless you were a medico: you had to be a ‘temporary typist’. I appealed to the Public Service Board, which came up and looked at all my research equipment – no typewriter – and said, ‘Yes, she’s a temporary typist.’ So from 1939 to ’42, that’s what I was. And every now and then the Chairman used to come through and say, ‘You are doing typing and shorthand, aren’t you, Gretna?’ I always changed the subject rapidly.

In 1941 I committed my second crime, I got married. (The first crime was being a temporary typist not able to type.) So of course I had to get out. Since war was on by then and things were pretty tough, I stayed home and had three children.

Tell us about your children.

They’ve all done science. The boy is an exploration geologist, for which he has worked all over the place. One girl is a cytogeneticist working in the haematology lab at the Hobart Hospital with leukaemia patients. Quite often it is found that their leukaemia is not cancer but is caused by an aberrant chromosome. She has to sort all that out: having worked out the patients’ chromosomes, with her staff she grows the platelets and the leucocytes, the white corpuscles, and other parts of their blood and works it all out.

The other daughter is now an embryologist in the UK, working for the IVF team at Leeds General Infirmary – their Dickensian name for a hospital! They inject a single sperm of a father-to-be into the mother’s egg – so it has the right parents – grow it and put it back in the woman. She then has her own baby, from her own egg and her husband’s sperm. That is proving very successful, as it needs to be: they don’t get paid unless a certain percentage of implants results in pregnancy. My daughter has been working in that field for some time and is in charge of the unit, even officially in charge, although it is in a hospital and she is not a doctor.

Like being a ‘temporary typist’ when you’re a scientist?

Exactly, yes – these hidebound ideas persist. Anyway, I continued to be needed at home. My husband had a tremendous lot of ill health and he had to retire early. He was ill for a long time before he died.

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Updating biology teaching

Caring for your husband as well as the three kids would seem to be a pretty full-time occupation, but you came back to the School of Botany. When did you do that?

In 1961 the Professor of Botany (Professor Turner), the Associate Professor (Dr McLennan) and the senior lecturer in mycology each rang me up separately and said, ‘We want you to come back now. Come back as a senior demonstrator and be prepared to do the lab work, set up the classes for Peter Thrower, and demonstrate in first-year biology, preparing all the material for the classes.’ I was told, ‘It’s a full-time job,’ and I said, ‘Oh – yes.’ Then, ‘You can go home after school when you haven’t got a class, and you can take the school holidays out of your annual leave.’ ‘Ohh,’ I said, ‘I’d love that!’ And then, ‘You’ll be expected to work for your PhD, any spare time you’ve got.’ To which I said, ‘O-o-oh, how wonderful!’ They could now give a PhD in Melbourne, which they hadn’t been able to do when I departed from Botany. So I went back.

I started off doing exactly what they said. But very soon I began lecturing in the Biology I course, going from assistant lecturer to lecturer to senior lecturer to reader to coordinator of biology, and I really enjoyed it. It was a big challenge: three lectures, one early in the morning – 9  o’clock – one at midday and one in the evening, 5.30 to 6.30, and big classes. And very often the prof had something else to do, so you had to take his lecture as well as yours.

In such a busy life, with things at home as well, you found room to make some great improvements on the descriptive botany of old.

Well, I instituted a number of changes in Biology I. For example, instead of the students just sitting doing descriptive work in the lab, I introduced little experiments whereby they had to measure things and draw conclusions from them. (And they always used to say, ‘What answers should we get?’) Also, I instituted tutorials on a problem basis. Each of the 15 or so students in the tutorial class had to write a paragraph on a problem I had set, to show whether they had understood the lectures. Then the demonstrator or lecturer taking the tute could go ahead, explaining what hadn’t been clearly understood. And I put in carrels for self-help for those that had got behind or not understood, or had missed classes.

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Why and how would take-all fungus infect Australian wheat?

What was the subject of your PhD research, and who was your supervisor?

Peter Thrower left to become professor in Hong Kong, so I didn’t have a supervisor. Professor Turner said, ‘I’ll be your supervisor, as long as you never come near me or ask me any questions, because I know nothing about your subject’ – which was take-all in wheat. That is a root fungus.

The farmers were having great problems. Whole bands of the field were ‘lodging’ (that is, the plants were collapsing) and the ears were ‘whiteheads’, they had no grain in them. A new virus, barley yellow dwarf, had just been discovered and people were not sure whether it or the take-all fungus was causing all this damage. This was part of my problem.

Robert Koch, last century, had established certain postulates: you had to isolate the fungus from a plant with the symptoms, you had to grow it separately on agar jelly, and then you had to put it back in a healthy plant, get the same symptoms and re-isolate. If you did all that, you fulfilled Koch’s postulates and you had proved your cause. I did it with the take-all fungus, which I found was causing the damage, not barley yellow dwarf. Take-all fungus was a worldwide problem in wheat fields. But why was it infecting these great swathes of wheat in Australia?

The old practice in farming all over the world had been to burn the stubble after a wheat crop, but farmers in Australia weren’t burning it, they were turning the sheep onto it. The sheep would eat the top and leave that stubble sitting there where the fungus was. I found that that fungus needs light to produce its spores. Using cross-gradients of light and temperature, I found it needed blue light of quite a high value, 3000 ergs per centimetre per second. And in the swathes in the paddock, with the stubble eaten down, it was certainly getting all the light it needed and so it was producing lots of spores.

How then was it infecting the new wheat crop? I got photographs of these spores being produced and demonstrated that they were infecting the new wheat crop – and I found it was producing certain enzymes which were killing the plants. They started to grow, but then they collapsed as the fungus took over their roots.

I’ve always based my research on asking a question, thinking up several possible explanations and devising experiments to find which one was right, with perhaps one final experiment to prove it, and then publishing it. So I put in my PhD thesis in 1968.

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Phytophthora cinnamomi: only a few dead grass trees, or the whole show?

Did you continue with the fungi, perhaps that same one?

Well, in 1970 Phytophthora cinnamomi, the cinnamon fungus, had been found in the Brisbane Ranges. Agriculture said, ‘Take-all is an agricultural problem. You do a botany problem,’ so I switched very happily to the cinnamon fungus. That’s where the jobs and the grants lay.

The cinnamon fungus affects 70 to 80 per cent of the understorey of our open forests, our dry sclerophyll forests. It cuts a great swathe through our native plants, killing them all. The grass trees are the most obvious: they just turn turtle. They go an orange–brown colour and collapse – looking like an old girl with a wig over her head. They don’t recover. And 45 per cent of the stringy-bark eucalypts die too, so it really has a very big effect. The fungus was causing great problems in jarrah in Western Australia, but in those days Western Australia seemed even further from Melbourne than now, and it wasn’t till 1965 that cinnamon fungus was isolated as the cause.

I took the research dignitaries from the Forest Commission up to see the disease in the Brisbane Ranges, but they laughed: ‘Fancy, Gretna’s worried about a few dead grass trees!’ Of course they were only interested in the trees, just as the Western Australians only considered jarrah. They didn’t worry about the understorey. I was worried about the whole show, a whole ecosystem, and specially any plants that are rare, or endemic, at risk of extinction. They’ve lost 17 Banksias in Western Australia due to the cinnamon fungus.

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Cinnamon fungus incursions: a result of disturbance or invasion?

Anyway, a group working in Canberra – ANU and CSIRO Plant Industry – said that the cinnamon fungus was a common soil component found in the soil everywhere, and the disease resulted from the forest being upset. They said bad management and disturbance – construction, roads, logging – were causing disease. When I went up to the Brisbane Ranges to look, I saw 70 to 80 per cent of the plants dead or dying, but healthy plants on the other side of a sharp boundary. The disease, the deaths, spread downhill in a swathe where the water went, and on either side of it was a completely healthy band. Thinking about all that, I decided it was much more like a foreign, infectious invader than disturbance, because I could see disturbance without any associated disease.

So I followed Koch’s postulates again. I isolated the fungus onto an agar jelly, I put it back into healthy seedlings and into healthy mature plants, and I got the symptoms and re-isolated the fungus. Then, with my spade, I dug a whole series of plots in the forest. In some I properly disturbed the soil; into others I put washed threads of the cinnamon fungus. A disturbance didn’t do any harm at all, no disease came. But where the washed threads of the cinnamon fungus had been added, disease symptoms appeared and spread downhill, and I could re-isolate downhill from it. (I did this in an area that was going to be infected anyway.)

You said you used ‘washed threads’. Did you grow up the fungus in the laboratory, wash it free of any nutrients and then put it into the soil so that you artificially introduced the fungus?

Yes – just carrying out Koch’s postulates, but in the field. The results absolutely proved that I was right, it was an overseas invader. With these results I got a research grant from the ARGC (the Australian Research Grants Committee), but unfortunately it was taken from the people in Canberra. They weren’t very pleased about that.

I took the matter to the Forest Commission, the National Parks and the shire engineers, and I published it and gave talks on it, because if the fungus was an infectious agent it was very important that we act immediately not to spread it, that we introduce hygiene. The Forest Commission and the National Parks believed me and took notice of what I said, but the shire engineers laughed in my face and took no notice, so that was that.

Then the Canberra group published an article – in a prestigious overseas journal – saying they’d found the fungus in an area that had never been disturbed by man. They gave a map reference, and then some bushwalkers from Canberra, mathematicians, exclaimed that it had cattle grazing and a goldmine in it, and a fire protection road through it. They said they knew the area well, and it wasn’t undisturbed bush. The editors of the overseas journal rang me up, and I had to support the mathematicians. That was a very unfortunate incident. I’m sorry for the group – now! – about it all.

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Where does the fungus come from, and how?

If we take it that we are dealing here with a pathogen that, like many of our pests, has been brought into the Australian ecosystem, how might it have come?

This would be speculation; I’ve not done any work on it. All the early pioneers who came to Australia brought their plants from home. That’s why we’ve all got English gardens. We don’t know what they brought in the soil or the roots. Also, Kelso (the conservator of forests) set up the first forestry plantations in Western Australia. In 1927 he established a pine plantation, but the pines just wouldn’t grow until some soil containing the right fungi for the roots – good fungi, that is – was brought in. But what else was brought in with it? Again we don’t know, do we? So those are two ways that pathogens could have come in. Thirdly, the cinnamon fungus doesn’t mind seawater. It was originally isolated from the mountains of Western Sumatra, Western Borneo, where it caused a decay, a canker, in the cinnamon tree, which is why it’s called cinnamon fungus. The zoo spores can swim in seawater and could have come over in a bit of debris. We’re not really far away from that area.

There are marine fungi. Another Phytophthora is the potato blight, but that only has one or two hosts, whereas the cinnamon fungus has a couple of thousand. And there are also quite harmless Phytophthoras which live in seawater.

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How does the disease spread (or fail to)?

What is the significance of the Wilsons Promontory invasion?

Well, after this we set up permanent plots, with controls, in the Brisbane Ranges, Wilsons Promontory and the Grampians, and at Narbethong – that has now been cultivated but the other areas are still there – and we still monitor them; last month we did the Grampians. From the plots we found out a whole lot of things about the way the disease spread and what harm it was doing. We isolated the fungus from the plots and watched the disease go from an aggressive phase of killing everything off, into resistant vegetation of sedges. Sedges and grasses are resistant – they simply form new roots when a root gets damaged, and don’t get a disease – and tea-tree’s partly resistant. The bush looked an absolute mess: no flowers, no honey, no pollen, just these sedges that are wind-pollinated (the pollen contains no nutrients), half-dead tea-tree, and grasses. That’s about it. Also there was a timber loss, so it was quite serious.

From Wilsons Promontory we know the story of how the disease got into all these national parks. In 1962 a low loader had been brought in, carrying a bulldozer to fight fires on the Five Mile Road. And the bulldozer, without being cleaned off, was parked in a gravel pit. But it had been in Yarram, where there was a lot of cinnamon fungus. The enemies to the cinnamon fungus are the soil micro-organisms, and we’ve done a lot of research on what happens: by virtue of numbers the microbial organisms eat the cinnamon fungus, antagonise it, compete with it and generally get rid of it if they can. But in a soil such as in the Brisbane Ranges, Wilsons Promontory and the Grampians there are very few soil microbes: in the Brisbane Ranges a gram of soil – which would cover about half of a five cent piece – contains only about 10,000 micro-organisms.

A question was bothering me, though: Why doesn’t the cinnamon fungus do its damage in the wet forests? It’s a water mould, it likes water. Why doesn’t it kill the mountain ash, which is susceptible? So I went up to the Forest Commission at Kallista and asked for somebody to show me all the dead trees in Sherbrooke Forest. A forester took me round to see them, and I noticed they’d all been killed by lightning – you could see the lightning scar down the trunk – until we got to Burnham Beeches, a garden area opposite Sherbrooke which has a lot of azaleas and rhododendrons, and they harbour the cinnamon fungus. (It doesn’t usually kill them, but it causes a lot of dieback and yellowing.) The swimming spores had come under the culvert, under the road that separates Burnham Beeches from Sherbrooke Forest, and it had killed six huge mountain ash there. The mountain ash were also suffering from soil compaction because cars had been parking there, and tree roots need air – oxygen – to absorb water and minerals.

The cinnamon fungus had spread into Sherbrooke just a little bit, and a sign was up: ‘Area being revegetated’. But we couldn’t isolate the fungus. That area has 1012 or 1014 micro-organisms per gram of soil, and they were providing a great biological control for the cinnamon fungus. That’s why it doesn’t grow in wet forests.

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The credit due to research students

By now I had research students, so all my findings from now on are with the help of research students. The papers have been published with their authorship as first author and they are a combination of the research students with me. So you have to give them all credit.

Indeed, one always does. Research students are a tremendously important part of the university experience and I always feel that people who have taken PhD students as their scholars have a second family.

They’re a delight. I’ve had great fun with my research students, especially as we all had to go up and look at these plots and do the recording. One of them used to bring his banjo and play bush ballads to us. They have remained mycologists: one is working in Western Australia, one is in Queensland, another is at Deakin University – they’ve gone to various jobs and they keep in touch.

You’ve obviously infected them very badly, Gretna.

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How does that dastardly fungus spread, survive and cause disease?

You have told us some ways this fungus can be spread, and something of the natural controls on it. What do you believe, however, from your collective studies, is the process by which these organisms affect an intact forest?

We asked ourselves: How are they spreading? How are they surviving? How are they causing disease? We found that usually the fungus is brought in on infected gravel which has no carbon content and therefore practically no micro-organisms in it – the fungus can survive very well, thank you, without any bacteria or other soil micro-organisms to compete with it. By growing the fungus in fabric brightener, on agar jelly, we could then see it, and we found that it produced swimming spores which were carried along in water and chemically attracted to any root. They would encyst on the root and then they’d produce a germ tube which was chemically attracted again into the root’s centre. All roots were penetrated by the fungus, but it didn’t produce disease in resistant plants like sedges or the resistant eucalypts. (The stringy-bark ash group are the only eucalypts susceptible to the disease.)

We wondered why the disease appears seasonally, in the spring and autumn. By continually measuring temperature and moisture content on all our plots, we found that the disease disappears in the cold of winter. Well, what happens to it? It disappears in the dry of summer. So, what happens to it? With the fabric brightener we could find out: it lives inside roots over the winter period and survives as resistant spores. It makes swimming spores which come in the spring, and resistant spores which come in the autumn.

How does the fungus make those two kinds of spores, and where?

The swimming spores are produced in spherical sporangia which form on the outside of the root only 24 hours after a root is infected, as long as the conditions are wet. Then they swim away and infect another root. They need water for forming, water for swimming and water for infection. But if they don’t find another root, they can produce a resistant spore in turn. The whole fungus’s life history is very adaptable; it can change according to conditions.

The resistant spores are produced inside the threads of the fungus, inside the root or in the soil. They can survive quite well in the soil. I’ve grown them in brightener, so they’re bright yellow or bright green, and planted them on little bits of nylon mesh in soil at various different water contents and in gravel and even in glass beads, and watched them: they produce lots more spores and threads of fungus, and some sporangia and some swimming spores. So the whole life cycle can take place for a short time without a host, as long as there are no soil microbes to compete with it.

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What does the fungus do to kill plants?

Perhaps you could tell us how the cinnamon fungus kills the plants.

This was a great worry to us. If you take a beautiful flowering gum, which is susceptible, cut off half its roots and stick it in soil, it will grow. But if you get one or two roots infected with the cinnamon fungus it dies. What does the cinnamon fungus do to kill such plants? They look as if they’re dying of drought.

We tested the roots, we watched their behaviour. The resistant plants encase the fungal threads in cork or wood – lignin – or callose, they encase the threads and so put the fungus out of action, and they make new roots. Sedges and grasses can continually make new roots, so they have no worry. But what happens in the susceptible plants? Well, the roots have membrane damage, so they leak a lot of nutrients and water out of them, and we found they increase their respiration rate. We examined all these things, and none of them answered.

Then one of my research students found that the roots lost their power to transport water, so the plants really were dying of drought after all. Within two days of infection, before any decay was evident, all water transport within the root was stopped – just like that. Measuring with pressure bombs and things, we found it was stopped. We tried two eucalypts for those experiments, and it didn’t happen with the resistant eucalypt, only with the susceptible. Another research student took over from there and he found how the cinnamon fungus had this far-reaching effect of stopping all water transport: it interfered with two hormones of the root, cytokinins and abscisic acid. And with modern molecular techniques, ELISA, he was able to measure the significant drop in these hormones.

That’s fascinating. I’ve noticed that when you see a set of infected trees collapse in a heap, it is almost always after about three days of very hot weather and then a really strong north wind. Boom, they’re gone.

Yes, the water stress plays a big part – because they’re dying of drought. In wet conditions they can keep on surviving.

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Dieback, then comeback: how does regeneration occur?

In the longer term, after an area has been infected and recovers to a very much more limited species distribution, does it ever regain any of its former diversity?

Yes, it does, although I must say I hadn’t expected it would. From 1970 to 1985, every second year we used to go up and survey all our plots in the various forests, and out of every single soil sample we took – 354, for instance, from the Grampians – we got Phytophthora. We have to bait for it, it’s not an easy thing to do, but we got 100 per cent from all the infected plots. (Nothing from the controls, of course.) Whether we surveyed the Grampians, the Brisbane Ranges or Wilsons Prom, it was the same: we got 100 per cent. And we also got it from all the different plots. So it was a dense population of pathogen and it was widely distributed. The plants just died off. The number of species declined, the cover declined, there was a lot of bare ground and the sedge. That was the aggressive phase and the disease then went into the resistant phase, with sedges and tea-trees – very boring looking.

Then it began to decline. From 1985 to 1994 we isolated the pathogen from, perhaps, only 15  per cent of the soil samples and of the plots. So there was less fungus and it was less widely distributed. And we got some regeneration, even though it was a very, very little bit. In 1994 I went up to the Brisbane Ranges, where Dr Ashton had set up big plots for his research students (for something quite different), and we measured 148 metres by 148 metres. It was very hard to isolate the fungus, but there were nine new Xanthorrhoeas – grass trees, an indicator plant – coming up in 9 years. And some other plants, not all, were back too.

From 1997 to 2000 there has been a massive regeneration, not only of the grass trees but of all the susceptible plants, including the ones we thought had disappeared. The seed must have been in the ground and they’ve all come up. The question is: Why? What’s doing this?

You may recall that the fungus was declining anyway. It had run out of susceptible roots to kill; it had no food supply and couldn't survive the winter and the dryness. But occasionally we’d still isolate it there. This amazing regeneration came up in amongst where the fungus was, and some of the plants got sick and died but others didn’t. We found dense regeneration, whole populations of susceptible plants. Maybe the soil micro-organisms had got extra active, but I think it’s the dryness. We have had three and a half years of drought, and the cinnamon fungus is a water mould, needing water to spread it. But our native plants are well adapted for dryness. If you try to grow Xanthorrhoea from seed, you’ve got to keep it practically dry, with no more than the slightest bit of moisture. It won’t tolerate wetness. So I think the dryness has benefited these plants and also discouraged the pathogen.

The only worry now is for the rare endemic plants. We’ve examined the ones in the Brisbane Ranges and found that of the six there, four are susceptible. I’ve got a new research student coming next month to replace a PhD student who has just finished, and we’re going to see how susceptible the endemics in the Grampians are.

I’m delighted to hear that latest piece of news. During your story of only sedges being left, I had been reminded rather sadly of La Belle Dame sans merci.

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Professional contributions

Gretna, over the years you have made quite a contribution to the phytopathology community in Australia and internationally. Would you tell us something of that?

International plant pathologists have never seen such a disease kill a whole forest, and they find it extraordinary. Overseas plants have evolved in competition with that fungus and developed resistance and so on, whereas it was new to ours and literally felled them. So I’ve given a lot of talks overseas and been invited to a lot of special conferences and to give review papers. I was the organising chairman of the Fourth International Plant Pathology Congress, in 1983, and I also organised a Phytophthora workshop at the University of Melbourne, to which we had about 2000 visitors. That was a lot of hard work – even though I had just retired.

That’s what you call retirement, is it!

And I got my DSc in that year. I put in a thesis with my published papers.

Congratulations. DSc by publication is a very great distinction.

I got the Medal of the Order of Australia in 1989, and then in 1989–90 I was asked to do a survey of the threat of the cinnamon fungus to the endemic floras right through each state of Australia. I spent a year or two doing this, going to each state, and I put in a very full report, 250 pages, which they’d guaranteed to publish. (I was not allowed to publish it.) But they never published it; it’s suppressed. I must have offended somehow – perhaps the West Australians didn’t want all their troubles exposed in this way. I’ve never asked what became of it but I think it is used as a resource. I’ve found that when you don’t publish, people use your results but they don’t feel they have to acknowledge them – great!

In 1994 the Australasian Plant Pathology Society, of which I was a foundation member, made me an honorary member and I had to write a review for their silver jubilee issue. And in 1999 I was made patron of the Australasian Mycological Society and they said I had to give a lecture as patron. Well, I have trouble remembering fungal names – I’m not a taxonomist, I never have been. So I rang up a cartoonist and asked could he draw a cartoon of an old girl with a sieve instead of a brain so that the fungal names went through, down into a black hole from which they just bounced up occasionally. He did that, without ever having seen me, and I showed that delightful cartoon in the lecture.

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Walking together

I hear you’re something of an organiser of walks. And a hip replacement a little time ago doesn’t seem to have stopped you walking.

Oh, I’ve had two hip replacements, most successful. I once broke an ankle bushwalking, and that was much more trouble. Anyway, in 1975, just after my husband died, the Melbourne University Staff Association approached me to lead a bushwalking group. Being coordinator of biology at that stage, I said yes, I would, provided they didn’t have any committees, any annual meetings, any annual reports, anything, but simply turned up on the walks – which I would lead. (I would do a reconnoitre first to make sure they were safe and it was walkable.) So for 22 years I did that, one walk a month. We took the university's overseas visitors and showed them the Australian bush, and I enjoyed that very much. We’re now having our 25th birthday, but we’ve expanded to include alumni and we have three leaders who take it in turns.

Finally, would you tell us about the amateur fungal researcher you assisted?

He’d been a motor mechanic, and he’d got the textbooks and bought himself a microscope. He really did some very good work on subterranean fungi and cup fungi. I’m no taxonomist, as I’ve said before, but I had to write his papers – otherwise, since he had no qualifications, they never would have been accepted. I got the references for him and I used to go up and visit him, but I didn’t do any of the actual work. There were 22 papers came out of that, which took a lot of my time. It was just another little bit of service to mycology, but it was worth doing.

What a great thrill for him, to have his work appropriately recognised in good journals. Thank you, Gretna, for talking to us about so many fascinating topics.

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