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The TSC22D, WNK, and NRBP gene families exhibit functional buffering and evolved with Metazoa for cell volume regulation.
Xiao, Yu-Xi; Lee, Seon Yong; Aguilera-Uribe, Magali; Samson, Reuben; Au, Aaron; Khanna, Yukti; Liu, Zetao; Cheng, Ran; Aulakh, Kamaldeep; Wei, Jiarun; Farias, Adrian Granda; Reilly, Taylor; Birkadze, Saba; Habsid, Andrea; Brown, Kevin R; Chan, Katherine; Mero, Patricia; Huang, Jie Qi; Billmann, Maximilian; Rahman, Mahfuzur; Myers, Chad; Andrews, Brenda J; Youn, Ji-Young; Yip, Christopher M; Rotin, Daniela; Derry, W Brent; Forman-Kay, Julie D; Moses, Alan M; Pritisanac, Iva; Gingras, Anne-Claude; Moffat, Jason.
Afiliación
  • Xiao YX; Program in Genetics and Genome Biology, The Hospital for Sick Children, Toronto, ON, Canada; Department of Molecular Genetics, University of Toronto, Toronto, ON, Canada.
  • Lee SY; Program in Genetics and Genome Biology, The Hospital for Sick Children, Toronto, ON, Canada.
  • Aguilera-Uribe M; Program in Genetics and Genome Biology, The Hospital for Sick Children, Toronto, ON, Canada; Department of Molecular Genetics, University of Toronto, Toronto, ON, Canada.
  • Samson R; Department of Molecular Genetics, University of Toronto, Toronto, ON, Canada; The Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Sinai Health, Toronto, ON, Canada.
  • Au A; Institute for Biomedical Engineering, University of Toronto, Toronto, ON, Canada; Department of Cell and Systems Biology, University of Toronto, Toronto, ON, Canada; Donnelly Centre, University of Toronto, Toronto, ON, Canada.
  • Khanna Y; Otto-Loewi Research Center, Division of Medicinal Chemistry, Medical University of Graz, Neue Stiftingtalstrabe 6, 8010, Graz, Austria.
  • Liu Z; Program in Cell Biology, The Hospital for Sick Children, Toronto, ON, Canada; Department of Biochemistry, University of Toronto, Toronto, ON, Canada.
  • Cheng R; Department of Molecular Genetics, University of Toronto, Toronto, ON, Canada; Program in Developmental and Stem Cell Biology, The Hospital for Sick Children, Toronto, ON, Canada.
  • Aulakh K; Program in Genetics and Genome Biology, The Hospital for Sick Children, Toronto, ON, Canada.
  • Wei J; Program in Genetics and Genome Biology, The Hospital for Sick Children, Toronto, ON, Canada.
  • Farias AG; Program in Genetics and Genome Biology, The Hospital for Sick Children, Toronto, ON, Canada; Department of Molecular Genetics, University of Toronto, Toronto, ON, Canada.
  • Reilly T; Program in Genetics and Genome Biology, The Hospital for Sick Children, Toronto, ON, Canada; Department of Molecular Genetics, University of Toronto, Toronto, ON, Canada.
  • Birkadze S; Program in Genetics and Genome Biology, The Hospital for Sick Children, Toronto, ON, Canada; Department of Molecular Genetics, University of Toronto, Toronto, ON, Canada.
  • Habsid A; Program in Genetics and Genome Biology, The Hospital for Sick Children, Toronto, ON, Canada.
  • Brown KR; Program in Genetics and Genome Biology, The Hospital for Sick Children, Toronto, ON, Canada.
  • Chan K; Program in Genetics and Genome Biology, The Hospital for Sick Children, Toronto, ON, Canada.
  • Mero P; Program in Genetics and Genome Biology, The Hospital for Sick Children, Toronto, ON, Canada.
  • Huang JQ; Department of Molecular Genetics, University of Toronto, Toronto, ON, Canada; Program in Molecular Medicine, The Hospital for Sick Children, Toronto, ON, Canada.
  • Billmann M; Institute of Human Genetics, School of Medicine and University Hospital Bonn, University of Bonn, 53127 Bonn, Germany.
  • Rahman M; Department of Computer Science and Engineering, University of Minnesota, Minneapolis, MN, USA.
  • Myers C; Department of Computer Science and Engineering, University of Minnesota, Minneapolis, MN, USA.
  • Andrews BJ; Department of Molecular Genetics, University of Toronto, Toronto, ON, Canada; Donnelly Centre, University of Toronto, Toronto, ON, Canada.
  • Youn JY; Department of Molecular Genetics, University of Toronto, Toronto, ON, Canada; Program in Molecular Medicine, The Hospital for Sick Children, Toronto, ON, Canada.
  • Yip CM; Institute for Biomedical Engineering, University of Toronto, Toronto, ON, Canada; Donnelly Centre, University of Toronto, Toronto, ON, Canada.
  • Rotin D; Program in Cell Biology, The Hospital for Sick Children, Toronto, ON, Canada; Department of Biochemistry, University of Toronto, Toronto, ON, Canada.
  • Derry WB; Department of Molecular Genetics, University of Toronto, Toronto, ON, Canada; Program in Developmental and Stem Cell Biology, The Hospital for Sick Children, Toronto, ON, Canada.
  • Forman-Kay JD; Department of Biochemistry, University of Toronto, Toronto, ON, Canada; Program in Molecular Medicine, The Hospital for Sick Children, Toronto, ON, Canada.
  • Moses AM; Department of Cell and Systems Biology, University of Toronto, Toronto, ON, Canada.
  • Pritisanac I; Otto-Loewi Research Center, Division of Medicinal Chemistry, Medical University of Graz, Neue Stiftingtalstrabe 6, 8010, Graz, Austria.
  • Gingras AC; Department of Molecular Genetics, University of Toronto, Toronto, ON, Canada; The Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Sinai Health, Toronto, ON, Canada.
  • Moffat J; Program in Genetics and Genome Biology, The Hospital for Sick Children, Toronto, ON, Canada; Department of Molecular Genetics, University of Toronto, Toronto, ON, Canada; Institute for Biomedical Engineering, University of Toronto, Toronto, ON, Canada. Electronic address: jason.moffat@sickkids.ca.
Cell Rep ; 43(7): 114417, 2024 Jul 23.
Article en En | MEDLINE | ID: mdl-38980795
ABSTRACT
The ability to sense and respond to osmotic fluctuations is critical for the maintenance of cellular integrity. We used gene co-essentiality analysis to identify an unappreciated relationship between TSC22D2, WNK1, and NRBP1 in regulating cell volume homeostasis. All of these genes have paralogs and are functionally buffered for osmo-sensing and cell volume control. Within seconds of hyperosmotic stress, TSC22D, WNK, and NRBP family members physically associate into biomolecular condensates, a process that is dependent on intrinsically disordered regions (IDRs). A close examination of these protein families across metazoans revealed that TSC22D genes evolved alongside a domain in NRBPs that specifically binds to TSC22D proteins, which we have termed NbrT (NRBP binding region with TSC22D), and this co-evolution is accompanied by rapid IDR length expansion in WNK-family kinases. Our study reveals that TSC22D, WNK, and NRBP genes evolved in metazoans to co-regulate rapid cell volume changes in response to osmolarity.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Tamaño de la Célula / Proteína Quinasa Deficiente en Lisina WNK 1 Límite: Animals / Humans Idioma: En Revista: Cell Rep Año: 2024 Tipo del documento: Article País de afiliación: Canadá
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Tamaño de la Célula / Proteína Quinasa Deficiente en Lisina WNK 1 Límite: Animals / Humans Idioma: En Revista: Cell Rep Año: 2024 Tipo del documento: Article País de afiliación: Canadá