期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 112, 期 4, 页码 1065-1070出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1415020112
关键词
Hippo; JNK; growth; Rho1; Drosophila
资金
- National Basic Research Program of China (973 Program) [2010CB944901, 2011CB943903]
- National Natural Science Foundation of China [31071294, 31171413, 31371490]
- PhD Programs Foundation of Ministry of Education of China [20120072110023]
- Shanghai Committee of Science and Technology [09DZ2260100, 14JC1406000]
The Hippo and c-Jun N-terminal kinase (JNK) pathway both regulate growth and contribute to tumorigenesis when dysregulated. Whereas the Hippo pathway acts via the transcription coactivator Yki/YAP to regulate target gene expression, JNK signaling, triggered by various modulators including Rho GTPases, activates the transcription factors Jun and Fos. Here, we show that impaired Hippo signaling induces JNK activation through Rho1. Blocking Rho1-JNK signaling suppresses Yki-induced overgrowth in the wing disk, whereas ectopic Rho1 expression promotes tissue growth when apoptosis is prohibited. Furthermore, Yki directly regulates Rho1 transcription via the transcription factor Sd. Thus, our results have identified a novel molecular link between the Hippo and JNK pathways and implicated the essential role of the JNK pathway in Hippo signaling-related tumorigenesis.
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