CIBSS Launchpad Funds Recipients 2025

Dr. Tanja Bhuiyan

Dr. Tanja Bhuiyan

Contact

Dr. Tanja Bhuiyan
Institute of Experimental and Clinical Pharmacology and Toxicology
University of Freiburg

T +49 761 203 96822
tanja.bhuiyan(at)pharmakol.uni-freiburg.de

Further Information

WWW

Selected publications:

  • Bhuiyan T.*,Arecco N., Mendoza Sanchez P.K., Kim J., Schwan C., Weyrauch S., Sheikh N., Prunotto A., Tekman M., Biniossek M.L., Knapp B., Koidl S., Drepper F., Huesgen P.F., Grosse R., Hugel T., Arnold S.J.* (2025), TAF2 condensation in nuclear speckles links basal transcription factor TFIID to RNA splicing factors. Cell Reports,Volume 44, Issue 5, 115616.  DOI: https://doi.org/10.1016/j.celrep.2025.115616, *corresponding authors
  • Sheikh N., Koidl S., Bhuiyan T., Werner T.V., Biniossek M.L., Bonvin A., Lassmann S., Timmers H.T.M. (2021) Integrating quantitative proteomics with accurate genome profiling of transcription factors by greenCUT&RUN. Nucleic Acids Research,Volume 49, Issue 9, Page e49., DOI: https://doi.org/10.1093/nar/gkab038

  • Bhuiyan T. and Timmers H.T.M. (2019), Promoter recognition: putting TFIID on the spot., Trends in Cell Biology, Volume 29, Issue 9, pages 752-763., DOI: https://doi.org/10.1016/j.tcb.2019.06.004

  • Kapuria V., Rohrig U.F., Bhuiyan T., Borodkin V.S., van Aalten D.M., Zoet, V., Herr, W. (2016), Proteolysis of HCF-1 by Ser/Thr glycosylation-incompetent O-GlcNAc transferase:UDP-GlcNAc complexes. Genes & Development, Volume 30, pages 960-972., DOI: https://doi.org/10.1101/gad.275925.115

  • Bhuiyan T., Waridel P., Kapuria V., Zoete V., Herr W. (2015), Distinct OGT-binding sites promote HCF-1 cleavage. PLoS ONE, Volume10, Issue 8, e0136636, DOI: https://doi.org/10.1371/journal.pone.0136636

  • Lazarus M.B., Jiang J., Kapuria V., Bhuiyan T., Janetzko J., Zandberg W.F., Vocadlo D.J., Herr W., Walker S. (2013) HCF-1 is cleaved in the active site of O-GlcNAc transferase. Science, Volume 342, No. 6163, pages 1235-1239, DOI: doi.org/10.1126/science.1243990

 

Functions of nuclear speckles during cellular stress and differentiation

Gene expression is regulated at multiple steps, from transcription initiation to pre-mRNA splicing and protein translation. Some of these steps occur in membraneless compartments, so-called biomolecular condensates. Nuclear speckles, or simply speckles, are biomolecular condensates in the cell nucleus of animals and plants occurring at varying sizes and numbers. In recent years, evidence has emerged for speckles to play an active role in gene regulation and yet, the molecular mechanisms underlying their regulatory functions remain unclear.

Variants of genes encoding speckle proteins can cause a variety of human developmental disorders, which are summarized as “speckleopathies”. These diseases comprise neurodevelopmental disorders or heart disease, highlighting the importance of speckles in these highly specialized cell types. Studying the speckle trajectory including speckle-regulated gene expression during states of cellular stress or from pluripotent to differentiated cells could advance our understanding of speckleopathies.

In this project, I will investigate protein shuttling between speckles and gene promoters and analyze the effects on transcription, promoter regulation, and RNA splicing in different cell states. I will first focus my studies on TAF2, a subunit of the basal transcription factor complex TFIID, which localizes to both speckles and gene promoters. My long-term research interest is to understand how dysregulation of speckles contributes to disease pathogenesis and investigate their potential as targets for pharmacological interventions.

Potential path of the TFIID subunit TAF2 through cellular compartments.
The microscopy image on the bottom left shows HeLa cells expressing TAF2 in nuclear speckle condensates. TAF2 translocates to the nucleus and associates with the basal transcription factor TFIID on chromatin (transcription compartment) or it accumulates in nuclear speckles (compartment associated with mRNA splicing). Schematic © Tanja Bhuiyan.