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Dr. Tao Wang’s group revealed that TBC1D7 regulates systemic growth in Drosophila

Publication Date:2018/03/09

On 29/11/2017, Dr. Tao Wang’s laboratory published a paper entitled “dTBC1D7 regulates systemic growth independently of TSC through insulin signaling” in Journal of Cell Biology. The authors found dTBC1D7 play a important role in regulating growth of Drosophila.

The tuberous sclerosis complex (TSC) is an essential node of the insulin/IGF signaling transduction pathway and negatively regulates cell growth through inactivation of the mechanistic target of rapamycin complex 1 (mTORC1). The TSC complex includes TSC1, TSC2 and TBC1D7, a new member recently identified. Somatic loss of heterozygosity in TSC1 or TSC2 leads to the occurrence of benign tumors in various organs while the loss of TBC1D7 is associated with megalencephaly. These divergent phenotypes imply that TBC1D7 has some important physiological functions that are distinct from its conventional TSC-complex-associated functions.

With the goal of dissecting the physiological roles of TBC1D7, the authors identified a homology of TBC1D7 in Drosophila, named dTBC1D7 and established a genetic model. By using Drosophila genetics and imaging technologies, Tao Wang’s group have characterized some native physiological functions of dTBC1D7 in Drosophila. In mutants lacking dTBC1D7, cells and organs growth are promoted in a cell-noautonomous and TSC-independent manner. dTBC1D7 is expressed in insulin-like peptides producing (IPC) cells in center neuron system of fly and control the biosynthesis and secretion of insulin-like peptides 2 (ILP2). Moreover, dTBC1D7 mutants were short-lived and accelerated aging processes due to elevation of circulating insulins.

Figure 1. dTBC1D7 mutants increased body size in pupae (A) and adult stage (B). Flies were dissected and immunostained for GFP (IPC cells) and ILP2 (red). High magnification pictures are shown in yellow frames. In dTBC1D7 mutants, ILP2 is a secretion-like pattern (C).

This work offers novel insights of the physiological functions of TBC1D7 in systemic control of growth as well as important implications of human disease caused by TBC1D7 mutation. Suxia Ren and Zengyi Huang from Tao Wang’ lab are the Co-first authors. Other contributing author includes Dr. Yuqiang Jiang from the Institute of Genetics and Developmental Biology (IGDB), Chinese Academy of Science. Dr. Tao Wang is the corresponding author. This project was supported by a grant of the 973 Program and the National Natural Science Foundation of China, and was carried out at the National Institute of Biological Sciences, Beijing.