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Understanding cell death in plants

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Matt Smith:

As the world's population rises and demand for food and bio-fuel increases, it has important implications for improving agricultural crop production. With me today is Professor Roger Parish, Head of the Botany Department and La Trobe University and he's been working on the problem of cell death in plants. Thank you for joining me Roger.

Roger Parish:

Thank you. A pleasure.

Matt Smith:

What is cell death in plants? How does it work?

Roger Parish:

Cell death can occur for two reasons. One is because, for example, a plant is attacked by a pathogen, a fungus or a bacterium, and the plant responds by the cells dying at the point of infection, and the dying cells prevent the spread of the pathogen and at the same time they're producing compounds that will actually kill the pathogen itself. So that's called death in response to infection. The other thing of course, everybody knows some plants are annuals and they die. That's season-related, but there are other aspects of cell death, which is the same as the development of the human embryo, some cells die very specifically and some of the cells even in a mature organism, according to a program. During the development of a plant for example, very specific cells have to die at a specific time and a specific place so the entire plant is produced, you know, the development of the different tissues occurs. So that happens in the human embryo etc.

Matt Smith:

OK. So it's a natural process. Why would it be beneficial to us if it worked in a different way? I'm assuming that if the cells of a plant get sick, you don't want that sickness to spread and you want cell death to occur.

Roger Parish:

That's correct. First of all, let's say we don't understand a lot about the molecular mechanisms underlying this cell death, be it programmed or not programmed. We do know that cells have large organelles called vacuoles – we have similar things in animals and those vacuoles are full on enzymes which can actually destroy a cell. They are like the digestive system of a cell really. As long as they're within this membrane which protects everything else – it's like a bag within the cell which contains the enzymes – and when that bag is ruptured, these enzymes are released into the rest of the cell and start breaking down the proteins and nucleic acids and so on, lipids, and the cell will die. Normally that's kept in the, if you like, the stomach of the cell and doesn't affect the rest of the cell. So one way in which cell death occurs is these vacuoles, the membranes break down and the cell dies, and that's very often what happens, say, during the attack by pathogens. The sort of cell death that we're looking at is a different one and the specific tissue we're interested in is something called the tapetum. The tapetum is a layer of cells within the developing anther and this layer of cells is absolutely essential for the production of pollen. What the layer of cells does – it produces molecules which become part of the pollen, out of all the pollen coat, and produces nutrients for the pollen developing in the middle of the anther. But this tapetum has to die at a certain time. If its death is premature, or its death is delayed, then the pollen doesn't develop properly and you have male sterility – you get no pollen. That's a very serious issue for the plant. One of the reasons we're particularly interested in this apart from understanding how this kind of cell death works, because it is a program, it's clearly a program, a genetic program, is that plants, particularly our crop plants, are very susceptible to what we call abiotic stress, that's cold, heat, dehydration and so on. And the tissue that is very sensitive is this tapetum. So we find for example, if the temperature's a bit low at the wrong time as the anther is developing, the tapetum's development is affected, the program is affected and you don't get the program cell death occurring at the right time, and in fact that cell death program isn't turned on and the tapetum doesn't die when it should. Because it doesn't die when it should, you get a male sterile plant, pollen isn't produced, and of course that has a dramatic effect on the yield of the crop. So the yield of the crop depends absolutely on the amount of pollen that's produced, and the health of that pollen. OK? So we're interested in the program that actually underlies this development of the tapetum. How does it develop? What are the genes involved? What are the genes that are specifically involved in that programmed cell death dying at the right time?

Matt Smith:

OK. So what exactly is the work that you've been doing then?

Roger Parish:

We've been looking at the genes that are involved in the development of the tapetum. It goes over a period of days. And we've identified genes which are absolutely critical for that development. One of those genes which we call MYB80, just for a name, carries a protein which regulates other proteins, and what we call a master switch. So that particular protein will turn on or off certain genes at a certain time. After discovering that protein, we've been interested in understanding the genes that it directly controls, and the way these transcription factors work, they bind to a specific gene and that turns that gene on, so now it's what we call transcribed and that means the production of a protein, transcribed and translated to give rise to a protein, the gene is expressed. So the MYB80 gene encodes from MYB80 protein, which then binds to and specifically activates certain genes. And we're interested in what those genes are. In our latest work we've identified a series of those genes and one of those genes turns out to be absolutely critical for the programmed cell death occurring at the specific time it needs to, in the tepetum.

Matt Smith:

What sort of plants is this effective on then?

Roger Parish:

We did our original work on the laboratory plant called Arabidopsis, which is a small thale cress plant, it's related to the brassicas such as canola and so on, and we have this gene not only in the brassicas, but in rice, wheat, barley, cotton – all of the crops that we've looked at, we've discovered this gene. It's highly conserved right across the spectrum as far as we can tell, and it's certainly in the crops that we're interested in, and certainly we know this system is functioning not only in Arabidopsis, but right across the spectrum of our crops, and if we knock out this gene, we get premature cell death. In other words, the cells die too early in the tapetum, and we get no pollen. So the question is, why is that happening, what's it doing? And we've discovered that one of the genes that it regulates is what we call a protease, a gene coating for a protein that breaks down other proteins. This gene is turned on by our MYB80 regulatory gene. So if we turn off that protease, which we call UNDEAD, if we turn off UNDEAD, just on its own so it isn't expressed, we can do that, then the cells die prematurely, exactly as they do as if you turn off MYB80. UNDEAD is produced and somehow stops the programmed cell death from occurring. Now that sounds counter intuitive because it's a breakdown – it breaks things down. You think, well, that would cause cell death, but what we believe it's doing is breaking down the specific proteins which is involved in the cell death, and that protein is then being made but it has to be broken down or the cells will die. And you want the cells to die, the plant wants the cells to die, at a very specific point. So the model that we think has evolved is that this programmed cell death is all ready to go, but as long as UNDEAD is being made, it stops it happening, because it's breaking down the protein. And the moment we turn off UNDEAD, MYB80 is turned off, or we turn it off, cell death can immediately occur. Another reason for believing that – if we change the system so UNDEAD can't be turned off, the cells don't die, in other words, they get bigger and bigger and bigger – you still get a male sterile plant but it's not due to cell death occurring too early – it's due to cell death not occurring at all, in the tepetum.

Matt Smith:

I'm going to use what's considered an evil word here by some – what you're essentially doing here is genetically modifying crops.

Roger Parish:

What we're currently doing is understanding the mechanism of programmed cell death. It's theoretically yes, if you want to apply this method, obviously to use this method to try and protect plants against the dangers of abiotic stress to ensure that pollen is made, first of all we have to understand exactly at what aspect for example the drought or the cold is working – it may be delaying the turning off of this gene, or it may be turning off early – we don't know that yet, you could then genetically engineer the tapetum in such a way that it is much more resistant to the cold effects. That's theoretically what one can do. And of course, yes, that will require some genetic engineering. And that will mean, genetically engineer crops and that will mean controversy.

Matt Smith:

What other characteristics of plants have you been looking at?

Roger Parish:

Because of the importance of this MYB80 gene in the regulation of pollen development, by turning that gene off specifically, we can obtain male sterile plants, otherwise they're quite normal, but they just don't make any seeds because they've got no pollen, and most of our crops are self-fertilising so they use their own pollen. So if we want to achieve plants with hybrid vigour, which I've talked about before, then we have to have a male sterile plant crossed with a, same species, plant but slightly different genetically, and then we get this type of vigour in the first generation, which can give rise to increases in productivity of thirty to fifty per cent, and that's probably one of the ways in which we're going to have to address the problem of food shortage, food security, in the next twenty to fifty years. We're probably not going to be able to increase productivity quickly enough to cover the increase in population if we don't use the hybrid vigour system, in my opinion. We've developed a method where we can actually do that – we can make one plant male sterile and we can cross it with the plant providing the pollen, and then we can reverse the system so that the next generation plant is no longer male sterile but it does have hybrid vigour. That's the way this system is relevant. The other thing we've been looking at is the role of these proteins in the development of the seed coat. We've got quite a big program looking at genes responsible for the formation of the seed and the seed coat – the seed coat is very important for protecting seed against environmental stress. I won't go into the details but we've got quite a lot of new information on that as well.

Matt Smith:

That's all the time we've got for the La Trobe University podcast today. If you have any questions, comments or feedback about this podcast, or any other, then send us an email at podcast@latrobe.edu.au. Roger Parish, thank you for your time today.

Roger Parish:

Thank you. A great pleasure.