Johnston, I.G. and Bassel, G.W. Identification of a bet-hedging network motif generating noise in hormone concentrations and germination propensity in Arabidopsis. Journal of the Royal Society Interface, 15 141 (2018)
Seeds feed the world, and uniform, reliable harvests of seeds and grains is essential for food security. However, there's a fundamental tension between the evolutionary priorities of plants and the agricultural priorities of humans. Evolutionarily, it is good for plants to "hedge their bets" by having seeds germinate at different times. A plant whose seeds all germinate in March will be susceptible to a frost in April, potentially leading to the loss of a generation of offspring. By contrast, a plant whose seeds germinate throughout March and April will have a subset of its offspring survive that frost, and its genes will be passed on to the next generation.
This bet-hedging poses a challenge for agriculture. In agricultural settings, we have more control over plant environments, and so plants have less need to withstand unpredictable environmental fluctuations. At the same time, non-uniform germination decreases crop yields, makes harvesting harder, and makes crops more susceptible to pest invasion. If we can learn how plants generate this evolved germination variability, we can design engineering and/or breeding strategies to reduce this and improve crop yields.
In a previous paper (blog post here), we looked at how germination is controlled by an interaction between two hormones known as ABA and GA. During that project, we noticed a surprising feature of the cellular pathways affecting ABA. Oddly, it seemed that ABA both activated a pathway that increased its own production, and at the same time (and in the same place) activated a pathways that increased its own degradation. These two pathways seemed to be competitive -- one increases levels of ABA, the other decreases them. Why would cells spend energy in this "futile" way?
We hypothesised that these competitive pathways might have the effect of generating variability in ABA levels. The pathways are fundamentally "noisy", involving random interactions in the chaotic environment of the cell. Consider increasing the activity of both pathways simultaneously. One pathway would act to increase levels of ABA, the other would act to decrease it. The increased "push and pull" of these noisy pathways would increase the spread of levels of ABA in different cells, even if average levels stayed the same.
Because it's hard to measure the levels of hormones in individual cells over time, we initially took a theoretical approach. We showed, with maths, that the competing pathways did indeed have this variability-inducing effect. By varying the activity through these pathways, the cell can increase variability in ABA levels, and hence increase variability in germination propensity. We showed that the theory we developed was compatible with some experiments where the ABA circuitry was artificially manipulated. The theory went on to reveal various aspects of cellular machinery that we could conceivably target through synthetic approaches, in order to reduce germination variability. Put together, our quantitative theory, supported by experiment, explained the mysterious competitive pathways and revealed several new interventions with the potential to improve food security. You can read about it for free in the Journal of the Royal Society Interface here. Iain
Seeds feed the world, and uniform, reliable harvests of seeds and grains is essential for food security. However, there's a fundamental tension between the evolutionary priorities of plants and the agricultural priorities of humans. Evolutionarily, it is good for plants to "hedge their bets" by having seeds germinate at different times. A plant whose seeds all germinate in March will be susceptible to a frost in April, potentially leading to the loss of a generation of offspring. By contrast, a plant whose seeds germinate throughout March and April will have a subset of its offspring survive that frost, and its genes will be passed on to the next generation.
This bet-hedging poses a challenge for agriculture. In agricultural settings, we have more control over plant environments, and so plants have less need to withstand unpredictable environmental fluctuations. At the same time, non-uniform germination decreases crop yields, makes harvesting harder, and makes crops more susceptible to pest invasion. If we can learn how plants generate this evolved germination variability, we can design engineering and/or breeding strategies to reduce this and improve crop yields.
Plants have evolved to "hedge their bets" by having seeds germinate at different times -- this makes generations of plants more robust to environmental fluctuations. Our work reveals a mechanism that "rolls dice" within plant cells, acting like a random number generator to produce variability in germination propensity.
In a previous paper (blog post here), we looked at how germination is controlled by an interaction between two hormones known as ABA and GA. During that project, we noticed a surprising feature of the cellular pathways affecting ABA. Oddly, it seemed that ABA both activated a pathway that increased its own production, and at the same time (and in the same place) activated a pathways that increased its own degradation. These two pathways seemed to be competitive -- one increases levels of ABA, the other decreases them. Why would cells spend energy in this "futile" way?
We hypothesised that these competitive pathways might have the effect of generating variability in ABA levels. The pathways are fundamentally "noisy", involving random interactions in the chaotic environment of the cell. Consider increasing the activity of both pathways simultaneously. One pathway would act to increase levels of ABA, the other would act to decrease it. The increased "push and pull" of these noisy pathways would increase the spread of levels of ABA in different cells, even if average levels stayed the same.
Because it's hard to measure the levels of hormones in individual cells over time, we initially took a theoretical approach. We showed, with maths, that the competing pathways did indeed have this variability-inducing effect. By varying the activity through these pathways, the cell can increase variability in ABA levels, and hence increase variability in germination propensity. We showed that the theory we developed was compatible with some experiments where the ABA circuitry was artificially manipulated. The theory went on to reveal various aspects of cellular machinery that we could conceivably target through synthetic approaches, in order to reduce germination variability. Put together, our quantitative theory, supported by experiment, explained the mysterious competitive pathways and revealed several new interventions with the potential to improve food security. You can read about it for free in the Journal of the Royal Society Interface here. Iain
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