Cells that are the building blocks of the organism come in different forms and functions. Stem cells are a unique type of cells, because of their ability to change (differentiate) or maintain their state. Because of this ability to differentiate into any type of cell, stem cells are on the frontiers of regenerative medicine, which is aimed to restore damaged cells, tissues or organs. The cell division (mitosis) poses a challenge for cell identity. During mitosis, the DNA is condensed into characteristic mitotic chromosomes, the nuclear membrane, separating DNA from rest of the cell, is fragmented, and the gene expression ceases. How then cells memorized which genes were expressed, to continue their expression after mitosis? The mitotic memory has been proposed as a mechanism for the maintenance of cell identity after mitosis. One arm of this mechanism, called bookmarking, is the binding of transcription factors (proteins regulating gene expression), to mitotic DNA. My research aims to establish the molecular mechanisms of mitotic bookmarking in mouse embryonic stem cells. Using methods, such as gene editing, genomics, and imaging, I am solving how stem cells maintain their identity after countless number of cell division.
Research Centres, Clusters, Institutes
- A TBP-independent mechanism for RNA Polymerase II transcription (2021)
- HSF2 protects against proteotoxicity by maintaining cell-cell adhesion (2018)
- HSP90 inhibitors disrupt a transient HSP90-HSF1 interaction and identify a noncanonical model of HSP90-mediated HSF1 regulation. (2018)
- Chaperone co-inducer BGP-15 inhibits histone deacetylases and enhances the heat shock response through increased chromatin accessibility. (2017)
Cell stress & chaperones,
- Stress management : multilayer regulation of the heat shock response (2017)
- Versatile functions of heat shock factors: It is not all about stress (2017)
Current Immunology Reviews, 13 (1), 4-18
- Uncoupling Stress-Inducible Phosphorylation of Heat Shock Factor 1 from Its Activation. (2015)
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