Issue date: 2024
Creative Commons Attribution 4.0 International (CC BY)
Cite as:
Ploss, Alexander, Berggren, Keith, Sinha, Saloni, Lin, Aaron, Schwoerer, Michael, Maya, Stephanie, Biswas, Abhishek, Cafiero, Thomas, Liu, Yongzhen, Gertje, Hans Peter, Suzuki, Saori, Berneshawi, Andrew, Carver, Sebastian, Heller, Brigitte, Hassan, Nora, Ali, Quzi, Beard, Daniel, Wang, Danyang, Cullen, John, Kleiner, Ralph, Crossland, Nicholas, & Schwartz, Robert. (2024). Mettl14-deletion related liver damage and nuclear heterotypia [Data set]. Princeton University.
  author      = {Ploss, Alexander and
                Berggren, Keith and
                Sinha, Saloni and
                Lin, Aaron and
                Schwoerer, Michael and
                Maya, Stephanie and
                Biswas, Abhishek and
                Cafiero, Thomas and
                Liu, Yongzhen and
                Gertje, Hans Peter and
                Suzuki, Saori and
                Berneshawi, Andrew and
                Carver, Sebastian and
                Heller, Brigitte and
                Hassan, Nora and
                Ali, Quzi and
                Beard, Daniel and
                Wang, Danyang and
                Cullen, John and
                Kleiner, Ralph and
                Crossland, Nicholas and
                Schwartz, Robert},
  title       = {{Mettl14-deletion related liver damage an
                d nuclear heterotypia}},
  publisher   = {{Princeton University}},
  year        = 2024,
  url         = {}

Liver-specific deletion of the N6-methyladenosine methyltransferase complex member, Mettl14, in a mouse model demonstrates progressive liver injury and marked nuclear heterotypia in hepatocytes. This phenotype correlates with significant changes in the transcriptomic profile relative to wild-type mouse liver, and changes in localization of the transcription / export machinery (TREX) complex as visualized by immunofluorescence. Mettl14 deletion liver also exhibits exacerbated injury to toxicity-based liver injury models, but shows no significant difference in regeneration after physical injury as modeled by partial hepatectomy. Deletion of the N6-methyladenosine recognizing proteins Ythdf1 and Ythdf2, both alone and together, impacts response to toxicity-based liver injury. This affects both liver mass regeneration and total mouse weight maintenance and recovery post-surgery. Dual deletion of Ythdf1 and Ythdf2 in liver tissue leads to liver damage in the steady state, and significantly exacerbated damage after liver injury models relative to either Ythdf1 or Ythdf2 deletion alone.

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1 readme.txt 36.2 KB
2 Mettl14_data_for_PDC.xlsx 3.13 MB