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Elucidating mechanisms underlying trait instability in maize

Project description

Paramutation and the processes behind crop trait instability

Crop trait instability, particularly under the pressures of climate change, presents risks to food security. Epigenetic mechanisms are increasingly recognised as key contributors to this instability. Paramutation is one of these mechanisms, whereby a silenced allele can suppress its active counterpart, leading to unstable traits across generations. Supported by the Marie Skłodowska-Curie Actions programme, the STEM project will deepen our understanding of how specific epigenetic modifications influence paramutation. The project will focus on the maize booster1 gene, exploring various hypotheses related to the interactions between DNA methylation and repressive histone modifications. These efforts will provide crucial insights into the mechanisms of paramutation, advancing our knowledge and offering potential strategies to stabilise desirable crop traits for future agricultural resilience.

Objective

Crop trait instability, particularly under climate change, poses a significant challenge to global food security. Epigenetic mechanisms are increasingly recognized as key contributors to this instability. Paramutation, an epigenetic phenomenon where one silenced inducing allele heritably silences its homologous active sensitive counterpart, leads to unstable traits across generations. Despite its implications for breeding, the mechanisms underlying paramutation remain largely elusive. Recent findings from the host lab suggest that specific DNA methylation and histone modification patterns play central roles in this process. Building on these insights, this project investigates how these epigenetic modifications influence paramutation, using the maize booster1 (b1) gene as a model.
The project is structured into two main objectives: First, I will investigate the hypothesis that inactive DNA flanking the sensitive b1 allele facilitates its silencing by the inducing b1 allele. If true, when exposed to the inducing allele, DNA methylation will spread from the inactive flanking DNA into the active b1 sequences, triggering their silencing. To test this, I will generate detailed DNA methylation profiles during key developmental stages using the novel Cas9-targeted long-read sequencing (nCATS) method. Second, I will explore the relationship between DNA methylation and repressive histone modifications, focusing on the order in which these epigenetic marks are established during paramutation. I will also employ the novel dCas12a-SunTag-TET1-system to specifically demethylate the flanking inactive regions of the active b1 allele, and assess its impact on paramutation. These approaches will advance our understanding of paramutation and provide clues on how to stabilise desirable crop traits. This project is a critical step toward my goal of becoming an independent researcher, by deepening my expertise in epigenetics, advanced lab techniques and crucial transferable skills.

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Topic(s)

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HORIZON-TMA-MSCA-PF-EF - HORIZON TMA MSCA Postdoctoral Fellowships - European Fellowships

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Call for proposal

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(opens in new window) HORIZON-MSCA-2024-PF-01

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Coordinator

UNIVERSITEIT VAN AMSTERDAM
Net EU contribution

Net EU financial contribution. The sum of money that the participant receives, deducted by the EU contribution to its linked third party. It considers the distribution of the EU financial contribution between direct beneficiaries of the project and other types of participants, like third-party participants.

€ 232 916,16
Total cost

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