Giuseppe Testa

  • Head of Neurogenomics
  • Research Group Leader, Testa Group

Giuseppe Testa, MD, PHD, MA, is a professor of Molecular Biology at Milan’s Università Statale and Director of the High Definition Disease Modelling Lab: Stem Cell and Organoid Epigenetics at the European Institute of Oncology. At Human Technopole, Prof. Testa leads the Neurogenomics centre of the research programme in collaboration with the Università Statale in Milan. The programme studies the molecular mechanisms underlying intellectual disabilities and autism.

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Publications

  • 10/2020 - Nature Communications

    JMJD3 acts in tandem with KLF4 to facilitate reprogramming to pluripotency

    The interplay between the Yamanaka factors (OCT4, SOX2, KLF4 and c-MYC) and transcriptional/epigenetic co-regulators in somatic cell reprogramming is incompletely understood. Here, we demonstrate that the histone H3 lysine 27 trimethylation (H3K27me3) demethylase JMJD3 plays conflicting roles in mouse reprogramming. On one side, JMJD3 induces the pro-senescence factor Ink4a and degrades the pluripotency regulator PHF20 in a […]

  • 09/2020 - Molecular Autism

    Autism spectrum disorder at the crossroad between genes and environment: contributions, convergences, and interactions in ASD developmental pathophysiology

    The complex pathophysiology of autism spectrum disorder encompasses interactions between genetic and environmental factors. On the one hand, hundreds of genes, converging at the functional level on selective biological domains such as epigenetic regulation and synaptic function, have been identified to be either causative or risk factors of autism. On the other hand, exposure to […]

  • 09/2020 - Nature

    LifeTime and improving European healthcare through cell-based interceptive medicine

    LifeTime aims to track, understand and target human cells during the onset and progression of complex diseases and their response to therapy at single-cell resolution. This mission will be implemented through the development and integration of single-cell multi-omics and imaging, artificial intelligence and patient-derived experimental disease models during progression from health to disease. Analysis of […]

  • 06/2020 - Molecular Autism

    The sociability spectrum: evidence from reciprocal genetic copy number variations

    Sociability entails some of the most complex behaviors processed by the central nervous system. It includes the detection, integration, and interpretation of social cues and elaboration of context-specific responses that are quintessentially species-specific. There is an ever-growing accumulation of molecular associations to autism spectrum disorders (ASD), from causative genes to endophenotypes across multiple functional layers; […]

  • 06/2020 - Neurosci Insights

    KMT2B and Neuronal Transdifferentiation: Bridging Basic Chromatin Mechanisms to Disease Actionability

    The role of bona fide epigenetic regulators in the process of neuronal transdifferentiation was until recently largely uncharacterized, despite their key role in the physiological processes of neural fate acquisition and maintenance. In this commentary, we describe the main findings of our recent paper “KMT2B is selectively required for neuronal transdifferentiation, and its loss exposes dystonia candidate […]