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Insulin/insulin-like growth factor signaling (IIS) plays a pivotal role in the regulation of growth at the cellular and the organismal level during animal development. Flies with impaired IIS are developmentally delayed and small due to fewer and smaller cells. In the search for new growth-promoting genes, we identified mutations in the gene encoding Lnk, the single fly member of the SH2B family of adaptor molecules. Flies lacking  lnk  function are viable but severely reduced in size. Furthermore,  lnk  mutants display phenotypes reminiscent of reduced IIS, such as developmental delay, female sterility, and accumulation of lipids. Genetic epistasis analysis places  lnk  downstream of the  insulin receptor  ( InR ) and upstream of  phosphoinositide 3-kinase  ( PI3K ) in the IIS cascade, at the same level as  chico  (encoding the single fly insulin receptor substrate [IRS] homolog). Both  chico  and  lnk  mutant larvae display a similar reduction in IIS activity as judged by the localization of a PIP 3  reporter and the phosphorylation of protein kinase B (PKB). Furthermore,  chico ;  lnk  double mutants are synthetically lethal, suggesting that Chico and Lnk fulfill independent but partially redundant functions in the activation of PI3K upon InR stimulation.

The Drosophila SH2B Family Adaptor Lnk Acts in Parallel to Chico in the Insulin Signaling Pathway