Image from Hudry et al, Nature (2016)
In our last journal club we discussed two very nice papers on sexual dimorphism in Drosophila intestines that controls growth, regeneration and lifespan:
The sexual identity of adult intestinal stem cells controls organ size and plasticity. Hudry B, Khadayate S, Miguel-Aliaga I. Nature. 2016 Feb 18;530(7590):344-8
Sex difference in pathology of the ageing gut mediates the greater response of female lifespan to dietary restriction. Regan JC, Khericha M, Dobson AJ, Bolukbasi E, Rattanavirotkul N, Partridge L. Elife. 2016 Feb 16;5. pii: e10956.
In the first paper, Bruno Hudry (from the lab of Irene Miguel Aliaga) showed that female intestines showed both a marked increase in cell proliferation/regeneration in response to damage and in increase propensity to develop tumors. Both these effects were dependent on the sexual identity of the intestinal stem cells, which is controlled by Transformer expression.
The second paper from Jenny Regan described male:female differences in both intestinal pathology in aged guts and response to infection. Interestingly, this paper indicates that these differences are regulated by the sexual identity of the differentiated epithelial cells in the gut, although the differences do involve altered stem cell proliferation.
We liked both papers a lot. Its a topic that we’ve become interested in – our former postdoc, Liz Rideout, recently published a paper on sex differences in insulin signaling and growth in Drosophila, and she’s continuing this work in her own lab at UBC.
In a recent lab journal club we discussed a very nice paper from Takashi Koyama and Christen Mirth:
Growth-Blocking Peptides As Nutrition-Sensitive Signals for Insulin Secretion and Body Size Regulation. (2016) PLoS Biology
Nutrients promote body growth in Drosophila by stimulating insulin signaling. One main way that this happens involves endocrine signaling between the fat body and the brain – in protein rich diets, amino acid import into fat body cells activates TOR and leads to release of a secreted factor(s) that acts on the brain to stimulate expression and release of insulin-like peptides (ILPs) from neurosecretory cells. However, the nature of the these AA-sensitive fat body factors has remained elusive. In this paper, the authors identify the Growth Blocking Peptides 1 and 2 (GBP1 and 2) as strong candidates. They show that expression of GBP1 and 2 is regulated by AA/TOR signaling and that both GBP1 and 2 are secreted from the fat body and can act directly on the brain to promote ILP release.
We liked this paper a lot. In particular we appreciated the rigorous and comprehensive approach the authors used to establish that both GBP1 and 2 are bona fide fat-body derived factors that respond to TOR signaling and that act directly on the brain to promote insulin release.