Yki can also act as an oncogene, since it has potent growth-promoting activity (reviewed in 13). The Hpo pathway limits organ size by phosphorylating and inhibiting Yki, a key regulator of proliferation and apoptosis. Yki is the key effector of growth control and the downstream element of the highly conserved Hpo (Hippo) signaling pathway. Here, we report a novel function for Cbt as a partner of Yki (Yorkie).

In spite of this, little is known about its downstream target genes or its precise mechanism of action.

Moreover, Cbt is a crucial downstream mediator gene of the JNK signaling required during wing disk regeneration 5. Among its functions, it is known that Cbt is required during dorsal closure downstream of JNK signaling 7, that it is a modulator of different signaling pathways involved in wing patterning and proliferation 11 and that it promotes ectopic cell cycling when overexpressed 12. Cbt levels rise upon inhibition of TOR signaling 8 9, and it is among the most highly Mlx-regulated genes 10. This TF is ubiquitously expressed in the wing disk, and its expression increases in response to metabolic, hormonal and stress signals. TIEG proteins participate in a wide variety of cellular processes, from development to cancer, and regulate genes that control proliferation, apoptosis, regeneration or differentiation 4 5.ĭrosophila cbt was identified and characterized from an overexpression screen of EP lines conducted to determine genes involved in establishing epithelial planar cell polarity 6 7. TIEGs are zinc finger proteins of the Krüppel-like factor (KLF) family that can function as either activators or repressors depending on the cellular context, the promoter to which they bind or the interacting partners 3. The transcription factor Cabut/dTIEG (Cbt) is the fly ortholog of TGF-β-inducible early genes 1 and 2 (TIEG1 and TIEG2) in mammals, which belong to the evolutionary conserved TIEG family 2. In fact, the final size and shape of an organism require a complex genetic network of signaling molecules, the final outcome of which must be finely regulated in space and time to ensure a proper response.

The combinatorial binding of transcription factors (TF) to these elements can lead to diverse types of transcriptional output, and an understanding of this mechanism is crucial, for example, in the context of development. Gene expression is regulated through the integrated action of, among others, many cis-regulatory elements, including core promoters and enhancers located at greater distances from transcription start sites (TSS) (reviewed in 1).

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