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Abstract
Size regulation is fundamental in developing multicellular organisms and occurs through
the control of cell number and cell size. Studies in Drosophila have identified an
evolutionarily conserved signaling pathway that regulates organismal size and that
includes the Drosophila insulin receptor substrate homolog Chico, the lipid kinase
PI(3)K (Dp110), DAkt1/dPKB, and dS6K.
We demonstrate that varying the activity of the Drosophila insulin receptor homolog
(DInr) during development regulates organ size by changing cell size and cell number
in a cell-autonomous manner. An amino acid substitution at the corresponding position
in the kinase domain of the human and Drosophila insulin receptors causes severe growth
retardation. Furthermore, we show that the Drosophila genome contains seven insulin-like
genes that are expressed in a highly tissue- and stage-specific pattern. Overexpression
of one of these insulin-like genes alters growth control in a DInr-dependent manner.
This study shows that the Drosophila insulin receptor autonomously controls cell and
organ size, and that overexpression of a gene encoding an insulin-like peptide is
sufficient to increase body size.