In a recent journal club, we discussed a paper from the Cagan lab: Transformed Drosophila cells evade diet-mediated insulin resistance through wingless signaling.
This paper continues with a theme from a previous lab journal club and describes how diet-induced changes in fly physiology can influence localized imaginal tissue growth caused by altered oncogene/tumor suppressor signaling pathways. Here, the Cagan lab show that rasv12/csk- clones show little or no growth phenotype in flies fed their ‘standard’ lab diet, but on a high sugar diet, these clones show massive overgrowth and invasive behaviour. The authors go on to show that this high sugar-phenotype can be explained in part by elevated Wg signaling in the rsv12/csk- cells, which leads to increased expression of the fly insulin receptor (InR) and increased insulin/PI3K signaling. Given that InR is also a transcriptional target of FOXO, we wondered whether some of the phenotype in RasV12/csk- may be explained by interactions with PI3K-FOXO signaling.
We liked this paper, which like the previous PTEN paper, is built upon an interesting finding that diet can interact with genotype to influence tissue growth. These two papers in particular illustrate the utility and power of fly genetics to explore how the micro and macro–environment can influence tissue growth.
One thought on “Lab Journal Club: Diet-induced insulin resistance and tumors in Drosophila”
Interesting, I would guess that dTORC1 mutants might also not hypertrophy in that manner. Will definitely have to take a read of it.
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