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Concept inventories, constructed based on an analysis of students' thinking and their explanations of scientific situations, serve as diagnostics for identifying misconceptions and logical inconsistencies and provide data that can help direct curricular reforms. In the current project, we distributed the Biological Concepts Instrument (BCI) to 17-18-year-old students attending the highest track of the Swiss school system (Gymnasium). Students' performances on many questions related to evolution, genetics, molecular properties and functions were diverse. Important common misunderstandings were identified in the areas of evolutionary processes, molecular properties and an appreciation of stochastic processes in biological systems. Our observations provide further evidence that the BCI is efficient in identifying specific areas where targeted instruction is required. Based on these observations we have initiated changes at several levels to reconsider how biological systems are presented to university biology studies with the goal of improving student's foundational understanding.

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.