Epigenetics of rare developmental disorders

Mutations in genes encoding the chromatin machinery are highly prevalent in neurodevelopmental disorders. Changes in chromatin packaging can modulate gene expression and in turn cellular functions. Our lab studies how these types of mutations affect not only the nucleus but also interactions between organelles, metabolism and the external environment. By investigating sex-based disease variability, cellular vulnerabilities linked to metabolic states and critical developmental windows, we untangle the complex landscape of chromatinopathies.

Experimental approaches and model systems

We use complementary approaches and methods, such as genome engineering (CRISPR/Cas9), transcriptomics, epigenomics (ChIP-seq, Cut&Tag), live and confocal microscopy, proteomics and biochemistry. We work with murine embryonic stem cells and human induced pluripotent stem cells (iPS), as well as various other mammalian cells and organoids. We also use the mouse model to validate our findings in complex systems.

Research website

Positions held

  • Since 12/2022: Group Leader, Institute for Human Genetics, University Medical Center (UMC), Mainz (HPG fellowship)
  • Since 05/2020: Senior Research Associate, Institute of Molecular Biology, Mainz
  • 2014-2020: Postdoctoral Fellow, MPI of Immunobiology & Epigenetics, Freiburg


  • 2014: PhD in Biology, University of Freiburg, Germany
  • 2009: MSc in Medical Biotechnology, University of Naples (Federico II), Italy

Selected publications by Felicia Basilicata

Basilicata MF, Keller Valsecchi CI. The good, the bad, and the ugly: Evolutionary and pathological aspects of gene dosage alterations. PLoS Genet. 2021;17(12):e1009906. Link

Valsecchi CIK*, Basilicata MF*, Georgiev P, Gaub A, Seyfferth J, Kulkarni T, Panhale A, Semplicio G, Manjunath V, Holz H, Dasmeh P, Akhtar A. RNA nucleation by MSL2 induces selective X chromosome compartmentalization. Nature. 2021;589(7840):137–142. Link

Basilicata MF, Bruel A-L, Semplicio G, Valsecchi CIK, Aktaş T, Duffourd Y, Rumpf T, Morton J, Bache I, Szymanski WG, Gilissen C, Vanakker O, Õunap K, Mittler G, van der Burgt I, El Chehadeh S, Cho MT, Pfundt R, Tan TY, Kirchhoff M, Menten B, Vergult S, Lindstrom K, Reis A, Johnson DS, Fryer A, McKay V, DDD Study, Fisher RB, Thauvin-Robinet C, Francis D, Roscioli T, Pajusalu S, Radtke K, Ganesh J, Brunner HG, Wilson M, Faivre L, Kalscheuer VM, Thevenon J, Akhtar A. De novo mutations in MSL3 cause an X-linked syndrome marked by impaired histone H4 lysine 16 acetylation. Nat. Genet. 2018 Sep 17. Link

Samata M, Alexiadis A, Richard G, Georgiev P, Nuebler J, Kulkarni T, Renschler G, Basilicata MF, Zenk FL, Shvedunova M, Semplicio G, Mirny L, Iovino N, Akhtar A. Intergenerationally Maintained Histone H4 Lysine 16 Acetylation Is Instructive for Future Gene Activation. Cell. 2020 Jun 3 Link

Basilicata MF, Frank M, Solter D, Brabletz T, Stemmler MP. Inappropriate cadherin switching in the mouse epiblast compromises proper signaling between the epiblast and the extraembryonic ectoderm during gastrulation. Sci. Rep. 2016;6:26562. Link