Elucidation of a universal size-control mechanism in Drosophila and mammals
Open accessAbstract
Coordination of cell proliferation and cell death is essential to attain proper organ size during development and for maintaining tissue homeostasis throughout postnatal life. In Drosophila, these two processes are orchestrated by the Hippo kinase cascade, a growth-suppressive pathway that ultimately antagonizes the transcriptional coactivator Yorkie (Yki). Here we demonstrate that a single phosphorylation site in Yki mediates the growth-suppressive output of the Hippo pathway. Hippo-mediated phosphorylation inactivates Yki by excluding it from the nucleus, whereas loss of Hippo signaling leads to nuclear accumulation and therefore increased Yki activity. We further delineate a mammalian Hippo signaling pathway that culminates in the phosphorylation of YAP, the mammalian homolog of Yki. Using a conditional YAP transgenic mouse model, we demonstrate that the mammalian Hippo pathway is a potent regulator of organ size, and that its dysregulation leads to tumorigenesis. These results uncover a universal size-control mechanism in metazoan.
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After YAP1 induction in transgenic mouse livers, expression levels of a number of genes associated with embryonic liver, including DIM, H19, and Afp, increased.
“Consistent with a previously published microarray analysis of YAP-TG-induced livers (Dong et al., 2007), the expression levels of a number of genes associated with embryonic liver, including DIM, H19, and Afp, increased after YAP1 induction.”
From Hippo Signaling Influences HNF4A and FOXA2 Enhancer Switching during Hepatocyte Differentiation (2014) · cites this paper as Dong et al., 2007
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Self-citation
- Authors
- Dong, J., Feldmann, G., Huang, J., Wu, S., Zhang, N., Comerford, S. A., Gayyed, M. F., Anders, R. A., Maitra, A., & Pan, D.
- Affiliations
- Johns Hopkins University (US)
- The University of Texas Southwestern Medical Center (US)
- Corresponding author
- Pan, Duojia
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2007-09
- Volume
- 130
- Issue
- 6
- Pages
- 1120-1133
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC2666353
- OpenAlex
- W2141595533
- Cited by
- 2,370
- References
- 2
- Citations by year
- 2026: 70 · 2025: 102 · 2024: 125 · 2023: 122 · 2022: 187 · 2021: 161 · 2020: 159 · 2019: 167 · 2018: 175 · 2017: 143 · 2016: 146 · 2015: 171 · 2014: 134 · 2013: 121 · 2012: 97
- FWCI
- 27.00
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 2146 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Eye Institute (EY015708, R01EY015708)
- National Cancer Institute (R01CA113669)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK081417, R21DK072532, DK067187, K08DK067187)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hippo pathway signaling and YAP/TAZ
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Keywords
- Hippo signaling pathway, Yorkie, YAP, organ size control, cell proliferation, cell death, nuclear localization, phosphorylation, growth inhibition, tissue homeostasis, carcinogenesis, Drosophila
- MeSH terms
- Serine-Threonine Kinase 3, YAP-Signaling Proteins, Hippo Kinases, Animals, Cell Line, Cell Nucleus, Cytoplasm, Doxorubicin, Drosophila, Homeostasis, Humans, Liver Neoplasms, Experimental, Mammals, Mice, Inbred C57BL, Mice, Transgenic, Mutation, Nuclear Proteins, Organ Size, Phosphorylation, Protein Kinases, Serine, Transcription Factors, Transfection, Signal Transduction, Trans-Activators, Apoptosis, Protein Serine-Threonine Kinases, Cell Cycle Proteins, Active Transport, Cell Nucleus, Large Neutral Amino Acid-Transporter 1, Drosophila Proteins, Intracellular Signaling Peptides and Proteins, Adaptor Proteins, Signal Transducing, Cell Proliferation, Mice
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