Transgenerational immune priming in plants

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In response to stress, plants and animals can exhibit rapid changes in their biology, enabling them to maximise their fitness. Exposure to stress can also generate long-term immunological 'memory', which enables the individual to develop faster and stronger defence responses to future exposures. Over recent years, evidence has accumulated that exposure of an individual to stress can also influence future stress responses in its offspring. Such effects are referred to as 'transgenerational', and are assumed to have evolved to maximise survival of an individual's gene pool in future generations, which are likely to encounter similar stresses.We recently made the important discovery that progeny from diseased plants are more resistant than genetically identical offspring from healthy plants. This increased resistance persisted over at least two stress-free generations, suggesting epigenetic inheritance. Resistant progeny did not show increased defence activity in the absence of pathogens, but instead exhibited an increased responsiveness of defence genes to infection. We therefore refer to this phenomenon as 'transgenerational immune priming' (TGIP), since progeny plants are 'primed' to respond more rapidly to infection. Importantly, we have begun to uncover the mechanisms underpinning this immunological plant memory, and discovered that TGIP is based on DNA methylation, a reversible DNA modification that can have a profound impact on gene activity without changes in DNA sequence.Transgenerational immune responses have important implications for natural plant populations, and present an opportunity for exploitation in sustainable agriculture. The ability to improve resistance to pests and diseases through epigenetic manipulation provides a new mechanism by which reliance on chemicals can be reduced without having to change the genetic make-up of our elite crop varieties.In this project, we will investigate the biological significance of TGIP and the molecular mechanisms behind it. Firstly, we will examine whether TGIP can be established when disease stress is experienced only by the maternal plant, or whether paternal tissues can also transmit priming information. This will provide clues as to how TGIP evolved and the mechanism by which it is established. As well as measuring the benefits of TGIP in terms of increased stress resistance in offspring, we will also identify where there are trade-offs: when priming against one form of stress has a negative impact on tolerance to another. Thus, we will employ different forms of stress (disease, herbivory, salinity) to induce TGIP in different parental lines, and then measure the degree of resistance to each of these different stresses in their progeny. These costs and benefits will be measured initially in terms of stress resistance phenotypes, but to add depth of understanding, we will follow up with assays to measure expression of a defined set of stress-responsive marker genes and use mass spectrometry to generate metabolite profiles. Finally, we will grow progeny lines from primed populations in competition to test for overall reproductive fitness benefits for TGIP.In parallel with these phenomenological studies, we will exploit next-generation sequencing technologies to identify the mechanisms involved in the establishment and maintenance of TGIP. Since long-term epigenetic changes in gene responsiveness are associated with DNA methylation, we will profile genome-wide DNA methylation patterns in control and primed plants. Thus, we will identify differentially-methylated regions linked to enhanced stress resistance. We have evidence that certain forms of small RNA molecule (siRNAs) known to regulate DNA methylation are important in establishing TGIP. Therefore, we will also profile siRNAs in control and primed plants to identify correlations between differentially expressed siRNAs and DNA methylation patterns.