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2015 ; 112
(4
): 1065-70
Nephropedia Template TP
Ma X
; Chen Y
; Xu W
; Wu N
; Li M
; Cao Y
; Wu S
; Li Q
; Xue L
Proc Natl Acad Sci U S A
2015[Jan]; 112
(4
): 1065-70
PMID25583514
show ga
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.
|Animals
[MESH]
|Drosophila Proteins/genetics/*metabolism
[MESH]
|Drosophila melanogaster
[MESH]
|Imaginal Discs/cytology/*embryology
[MESH]
|Intracellular Signaling Peptides and Proteins/genetics/*metabolism
[MESH]
|JNK Mitogen-Activated Protein Kinases/genetics/*metabolism
[MESH]