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Figure 10 | BMC Developmental Biology

Figure 10

From: Loss of the Drosophila cell polarity regulator Scribbled promotes epithelial tissue overgrowth and cooperation with oncogenic Ras-Raf through impaired Hippo pathway signaling

Figure 10

Model for how the loss of scrib affects Hippo pathway signaling. In an epithelial cell, the core Hippo pathway components Hpo (H), Wts (W), Sav (S) and Mats (M) inhibit the activity of Yki, which acts to regulate transcription through its DNA binding partner, Sd. Extracellular regulation of the pathway occurs through the two transmembrane proteins, Crb acting through Ex, and Ft, acting through both Ex and D. Ex can also directly bind to and inhibit Yki. Loss of scrib in the eye disc is associated with aPKC-dependent inhibition of the Hippo pathway. Although JNK signaling is activated by either the loss of scrib, or ectopic aPKC activity, JNK is not required for Hippo pathway inhibition. In the wing disc, loss of scrib is also associated with JNK activation, and although JNK signaling has been shown to be sufficient to downregulate the Hippo pathway in the wing disc [37], Hippo pathway signaling remains impaired in scrib mutants even when JNK is blocked. Epistasis experiments suggest that pathway inhibition in scrib mutants occurs, at least in part, downstream or in parallel to Ex and Ft, and could impact upon either the core components (H/S/M/W) or upon Yki activity itself.

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