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@ARTICLE{Wang:299792,
      author       = {R. Wang and M. Roiuk$^*$ and F. Storer and A. A.
                      Teleman$^*$ and M. Amoyel},
      title        = {{S}ignals from the niche promote distinct modes of
                      translation initiation to control stem cell differentiation
                      and renewal in the {D}rosophila testis.},
      journal      = {PLoS biology},
      volume       = {23},
      number       = {3},
      issn         = {1544-9173},
      address      = {Lawrence, KS},
      publisher    = {PLoS},
      reportid     = {DKFZ-2025-00547},
      pages        = {e3003049 -},
      year         = {2025},
      abstract     = {Stem cells have the unique ability among adult cells to
                      give rise to cells of different identities. To do so, they
                      must change gene expression in response to environmental
                      signals. Much work has focused on how transcription is
                      regulated to achieve these changes; however, in many cell
                      types, transcripts and proteins correlate poorly, indicating
                      that post-transcriptional regulation is important. To assess
                      how translational control can influence stem cell fate, we
                      use the Drosophila testis as a model. The testis niche
                      secretes a ligand to activate the Janus kinase (JAK)/signal
                      transducer and activator of transcription (STAT) pathway in
                      two stem cell populations, germline stem cells (GSCs) and
                      somatic cyst stem cells (CySCs). We find that global
                      translation rates are high in CySCs and decrease during
                      differentiation, and that JAK/STAT signaling regulates
                      translation. To determine how translation was regulated, we
                      knocked down translation initiation factors and found that
                      the cap binding complex, eIF4F, is dispensable in
                      differentiating cells, but is specifically required in CySCs
                      for self-renewal, acting downstream of JAK/STAT activity.
                      Moreover, we identify eIF3d1 as a key regulator of CySC
                      fate, and show that two eIF3d1 residues subject to
                      regulation by phosphorylation are critical to maintain CySC
                      self-renewal. We further show that Casein Kinase II (CkII),
                      which controls eIF3d1 phosphorylation, influences the
                      binding of eIF3d and eIF4F in mammalian cells, and that CkII
                      expression is sufficient to restore CySC function in the
                      absence of JAK/STAT. We propose a model in which niche
                      signals regulate a specific translation programme in which
                      only some mRNAs are translated. The mechanism we identify
                      allows stem cells to switch between modes of translation,
                      adding a layer of regulation on top of transcription and
                      providing cells with the ability to rapidly change gene
                      expression upon receiving external stimuli.},
      cin          = {B140},
      ddc          = {610},
      cid          = {I:(DE-He78)B140-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40067813},
      doi          = {10.1371/journal.pbio.3003049},
      url          = {https://inrepo02.dkfz.de/record/299792},
}