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@ARTICLE{Ansari:277410,
      author       = {I. Ansari and L. Solé-Boldo$^*$ and M. Ridnik and J.
                      Gutekunst$^*$ and O. R. Gilliam$^*$ and M. Korshko and T.
                      Liwinski and B. Jickeli and N. Weinberg-Corem and M.
                      Shoshkes-Carmel and E. Pikarsky and E. Elinav$^*$ and F.
                      Lyko$^*$ and Y. Bergman},
      title        = {{TET}2 and {TET}3 loss disrupts small intestine
                      differentiation and homeostasis.},
      journal      = {Nature Communications},
      volume       = {14},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2023-01364},
      pages        = {4005},
      year         = {2023},
      note         = {DKFZ-ZMBH Alliance / #EA:A130# / #DKFZ-MOST-Ca200#},
      abstract     = {TET2/3 play a well-known role in epigenetic regulation and
                      mouse development. However, their function in cellular
                      differentiation and tissue homeostasis remains poorly
                      understood. Here we show that ablation of TET2/3 in
                      intestinal epithelial cells results in a murine phenotype
                      characterized by a severe homeostasis imbalance in the small
                      intestine. Tet2/3-deleted mice show a pronounced loss of
                      mature Paneth cells as well as fewer Tuft and more
                      Enteroendocrine cells. Further results show major changes in
                      DNA methylation at putative enhancers, which are associated
                      with cell fate-determining transcription factors and
                      functional effector genes. Notably, pharmacological
                      inhibition of DNA methylation partially rescues the
                      methylation and cellular defects. TET2/3 loss also alters
                      the microbiome, predisposing the intestine to inflammation
                      under homeostatic conditions and acute inflammation-induced
                      death. Together, our results uncover previously unrecognized
                      critical roles for DNA demethylation, possibly occurring
                      subsequently to chromatin opening during intestinal
                      development, culminating in the establishment of normal
                      intestinal crypts.},
      cin          = {A130 / F220},
      ddc          = {500},
      cid          = {I:(DE-He78)A130-20160331 / I:(DE-He78)F220-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37414790},
      doi          = {10.1038/s41467-023-39512-3},
      url          = {https://inrepo02.dkfz.de/record/277410},
}