Lab Journal Club: A holidic diet for Drosophila Melanogaster

In our last lab journal club, we discussed the recent paper from Matt Piper (@piperlab) (along with the Ribeiro (@RibeiroLab), Partridge and Pletcher labs) in which they define a holidic diet for Drosophila research:

A holidic medium for Drosophila Melanogaster (2013) Nat Methods

Variations in fly food between different labs (and even within labs) can profoundly influence organismal phenotypes, particularly behavioural, lifespan and stress responses. So, this very nice, meticulous paper provides an important, defined set of dietary conditions upon which to carry out these type of experiments.

As larval growth researchers, we were particularly interested in the finding that on the holidic diet, larvae took several days longer to pupate than on a ‘normal’ yeast/sugar-based food. Moreover, this delayed development could be abrogated by adding a small amount of yeast extract to the holidic diet. So what is the magic yeast ingredient?  A gustatory cue? An olfactory cue?  – (given the recent paper from the Banerjee lab – coming up next on lab journal club – on how olfactory cues can influence physiological responses in larvae). Also Or83B (olfactory receptor) mutant larvae show a (modest) delay in development, which is more pronounced when they have to compete with wildtype flies to forage for food (from – Vosshall lab @pollyp1)

Lab Journal Club: Diet-induced insulin resistance and tumors in Drosophila

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.