Finally, my latest paper is out. Took a lot to get it accepted, but in the end it came out rather well, I think. From the current issue of Development: (requires subscription for full article)

Insulin signaling promotes germline proliferation in C. elegans

1. David Michaelson,
2. Dorota Z. Korta,
3. Yossi Capua and
4. E. Jane Albert Hubbard

Summary

Cell proliferation must be coordinated with cell fate specification during development, yet interactions among pathways that control these two critical aspects of development are not well understood. The coordination of cell fate specification and proliferation is particularly crucial during early germline development, when it impacts the establishment of stem/progenitor cell populations and ultimately the production of gametes. In C. elegans, insulin/IGF-like receptor (IIR) signaling has been implicated in fertility, but the basis for the fertility defect had not been previously characterized. We found that IIR signaling is required for robust larval germline proliferation, separate from its well-characterized role in preventing dauer entry. IIR signaling stimulates the larval germline cell cycle. This activity is distinct from Notch signaling, occurs in a predominantly germline-autonomous manner, and responds to somatic activity of ins-3 and ins-33, genes that encode putative insulin-like ligands. IIR signaling in this role acts through the canonical PI3K pathway, inhibiting DAF-16/FOXO. However, signaling from these ligands does not inhibit daf-16 in neurons nor in the intestine, two tissues previously implicated in other IIR roles. Our data are consistent with a model in which: (1) under replete reproductive conditions, the larval germline responds to insulin signaling to ensure robust germline proliferation that builds up the germline stem cell population; and (2) distinct insulin-like ligands contribute to different phenotypes by acting on IIR signaling in different tissues.

Basically, what this means is that we analyzed a role for insulin-like signaling in the development of the reproductive system. The ability of the reproductive system to produce abundant germ cells (the worm produces both sperm and eggs and we didn't examine them individually) is controlled both by the pool of cells that are kept from differentiating into mature germ cells and thus can continue to to divide, as well as by the rate at which those cells divide. The first aspect is controlled primarily by a signaling pathway called "Notch" and the second aspect is controlled primarily by an insulin signaling pathway, though based on other work it may ultimately prove that both pathways may be controlling distinct aspects of the cell division cycle (the orderly process of one cell dividing into two cells) of the germ cells.

This work dovetails nicely with excellent work done in fruit flies: (from a 2008 PNAS article)

Insulin levels control female germline stem cell maintenance via the niche in Drosophila

1. Hwei-Jan Hsu and
2. Daniela Drummond-Barbosa1

Abstract

Stem cell maintenance depends on local signals provided by specialized microenvironments, or niches, in which they reside. The potential role of systemic factors in stem cell maintenance, however, has remained largely unexplored. Here, we show that insulin signaling integrates the effects of diet and age on germline stem cell (GSC) maintenance through the dual regulation of cap cell number (via Notch signaling) and cap cell–GSC interaction (via E-cadherin) and that the normal process of GSC and niche cell loss that occurs with age can be suppressed by increased levels of insulin-like peptides. These results underscore the importance of systemic factors for the regulation of stem cell niches and, thereby, of stem cell numbers.