09.09.2024

DFG: Priority Programme “EPIADAPT: Epigenomic Adaptations of the Developing Neural Chromatin”

Deadline: 11 December 2024

Epigenetic chromatin modifications extend the repertoire of gene expression control mediated by a plethora of transcription factors. In development, epigenetic features can be transmitted from stem cells to differentiated progeny, modify cell fate decisions and establish an epigenetic memory of early lifetime experiences. The inheritance of epigenetic modifications emerges as a mechanism for how environmental signals leave traces in the chromatin. In central nervous system (CNS) development, epigenetics mediates adaptive changes in gene expression that accompany or drive cell state conversions. Because they can be stable or dynamic, triggered by environmental factors or genetic mutations/variations, altered epigenetic signatures contribute to human brain diseases with an origin in early life. To advance knowledge of the basic mechanisms of CNS development, the physiological responses during adaptation and their deregulation in developmental diseases and upon environmental insults, it is essential to investigate the molecular repertoire connecting mechanistically cellular features, transcriptional responses, epigenetic processes and environmental signals that together orchestrate CNS development.

Neuroepigenetics in particular advances basic knowledge of epigenetic gene expression control in the context of terminally differentiated neural cells with a long lifespan. It reveals how the neural chromatin integrates continuously changing conditions and exposes molecular mechanisms of brain cell specification and adaptation. It clarifies the setting in which chromatin regulation drives development and in which altered chromatin follows instructive environmental stimuli during cell state transitions. The focused research on the adaptive neural epigenome in the SPP EPIADAPT aims to explore the causalities of epigenomic adaptations during development by gaining an understanding of signalling to and from neural chromatin and by connecting adapted epigenomes to cellular outcomes. 

The objectives of the SPP EPIADAPT are:

1. to identify relevant biological mechanisms that mediate epigenomic adaptation through specific epigenetic writers, readers and erasers or remodellers; 
2. to explore molecular alterations in the different cellular compartments in the environment-epigenome signal transduction cascade active during development; and 
3. to characterise the dynamics of epigenomes in the developing central nervous system (CNS) linked to cellular phenotypes that define epigenetic barriers, permissive epigenomes and target specificity, ideally with single-cell or cell-type resolution.

The insights to be delivered within the funding period  molecular mechanisms that mediate the environmental contribution to an adapted neuroepigenome and control the plasticity of the neuroepigenome during progression of development. Projects aiming to explore epigenomic adaptations in the developing neural chromatin must imperatively include:

• Multiomic approaches to study epigenetic mechanisms (i.e., DNA methylation, histone modifications, chromatin accessibility, 3D genome organisation) in neural progenitors/stem cells, neurons and/or glia, in at least two different developmental states, to define adapted epigenomes, their cause and/or consequence; and
• Integrative data analyses advancing multiomics and multiscale views, with the aim to resolve mechanistic interdependencies of cell-specific epigenomes during developmental adaptation, ideally at single-cell or cell-type specific resolution; and
• Experimental efforts to understand mechanistically the plasticity of the neuroepigenome, to resolve whether or when the epigenome follows or allows development; and
• Data analysis and/or experimental attempts to resolve the connection between altered epigenomes and activity of signalling pathways; and 
• Relevant model systems restricted to humans or mice (iPSC-, ESC-derived neural progenitors, neurons, or glia, primary cell culture models with at least one CNS-derived cell type, brain organoids, human or mouse brain tissue).

In addition, to advance neuroepigenomic research further, there are other criteria that must be met. See the full call here:
https://www.dfg.de/de/aktuelles/neuigkeiten-themen/info-wissenschaft/2024/ifw-24-79 

Proposals must be written in English and submitted to the DFG by 11 December 2024.

The DFG strongly welcomes proposals from researchers of all genders and sexual identities, from different ethnic, cultural, religious, ideological or social backgrounds, from different career stages, types of universities and research institutions, and with disabilities or chronic illness. With regard to the subject-specific focus of this call, the DFG encourages female researchers in particular to submit proposals.

More information:
https://uni-freiburg.de/spp2502 

Online EPIADAPT symposium:
Interested applicants are invited to participate and discuss their project ideas at the online EPIADAPT symposium on 1 October 2024. Please register by sending an email until 25 September 2024 with a title and abstract of your 10-minute presentation to:
spp2502spam prevention@mail.uni-freiburg.de 

For scientific enquiries, please contact the Priority Programme coordinator:
Professor Dr. Tanja Vogel
Albert-Ludwigs-Universität Freiburg
Institut für Anatomie und Zellbiologie
Anatomie II: Abteilung für Molekulare Embryologie
phone +49 761 203 5086
spp2502spam prevention@mail.uni-freiburg.de 

Questions on the DFG proposal process can be directed to:
Programme contact:
Dr. Thomas Baumgarten
phone +49 228 885-2456
thomas.baumgartenspam prevention@dfg.de

Administrative contact:
Alexandra Schäpe
phone +49 228 885-3087
alexandra.schaepespam prevention@dfg.de