Abstract
Organ size is regulated by intercellular signaling for cell growth and proliferation. The TOR pathway mediates a key signaling mechanism for controlling cell size and number in organ growth. Chaperonin containing TCP-1 (CCT) is a complex that assists protein folding and function, but its role in animal development is largely unknown. Here we show that the CCT complex is required for organ growth by interacting with the TOR pathway in Drosophila. Reduction of CCT4 results in growth defects by affecting both cell size and proliferation. Loss of CCT4 causes preferential cell death anterior to the morphogenetic furrow in the eye disc and within wing pouch in the wing disc. Depletion of any CCT subunit in the eye disc results in headless phenotype. Overgrowth by active TOR signaling is suppressed by CCT RNAi. The CCT complex physically interacts with TOR signaling components including TOR, Rheb, and S6K. Loss of CCT leads to decreased phosphorylation of S6K and S6 while increasing phosphorylation of Akt. Insulin/TOR signaling is also necessary and sufficient for promoting CCT complex transcription. Our data provide evidence that the CCT complex regulates organ growth by directly interacting with the TOR signaling pathway.
Highlights
Organ size is regulated by intercellular signaling for cell growth and proliferation during development
TRiC/Chaperonin containing TCP-1 (CCT) chaperonins are essential for organ growth by interacting with insulin/TOR signaling in
We have shown that the CCT complex is essential for the regulation of cell growth, proliferation, and survival during Drosophila organ development by Depletion of any CCT subunit by ey-Gal4 resulted in loss of larval eye disc and the headless phenotype in adults (Figs. 1 and 4f), implying that CCT is required during early stages of eye-head development
Summary
Organ size is regulated by intercellular signaling for cell growth and proliferation during development. The insulin/ TOR signaling pathway is a highly conserved mechanism for controlling cell and organismal growth [1, 2]. This pathway is activated in response to a variety of environmental cues such as nutrients, hypoxia, osmotic stress, and DNA damage [3]. Insulin signaling leads to activation of TOR kinase through signal transduction steps including PI3K, Akt, and Rheb. Activated TOR phosphorylates its targets S6K and 4E-BP to promote cell growth and .
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