Companion Blood Cells Control Ovarian Stem Cell Niche Microenvironment and Homeostasis.

The extracellular matrix plays an essential role for stem cell differentiation and niche homeostasis. Yet, the origin and mechanism of assembly of the stem cell niche microenvironment remain poorly characterized. Here, we uncover an association between the niche and blood cells, leading to the formation of the Drosophila ovarian germline stem cell niche basement membrane. We identify a distinct pool of plasmatocytes tightly associated with the developing ovaries from larval stages onward. Expressing tagged collagen IV tissue specifically, we show that the germline stem cell niche basement membrane is produced by these "companion plasmatocytes" in the larval gonad and persists throughout adulthood, including the reproductive period. Eliminating companion plasmatocytes or specifically blocking their collagen IV expression during larval stages results in abnormal adult niches with excess stem cells, a phenotype due to aberrant BMP signaling. Thus, local interactions between the niche and blood cells during gonad development are essential for adult germline stem cell niche microenvironment assembly and homeostasis.

Asymmetric localisation of cytokine mRNA is essential for JAK/STAT activation during cell invasiveness.

The transition from immotile epithelial cells to migrating cells occurs in all organisms during normal embryonic development, as well as during tumour metastasis. During Drosophila oogenesis, border cells (BCs) are recruited and delaminate from the follicular epithelium. This process is triggered by the polar cells (PCs), which secrete the cytokine Unpaired (Upd) and activate the JAK/STAT pathway in neighbouring cells, turning them into invasive BCs. Interestingly, either a decrease or an increase in BC number alters migration, indicating that mechanisms controlling the level of JAK/STAT signalling are crucial in this process. Here, we show that PCs have a highly stable and polarised network of microtubules along which upd transcripts are asymmetrically transported in a Dynein-dependent manner. We demonstrate that in the absence of upd mRNA localisation the ligand is no longer efficiently secreted, leading to a loss of signalling strength as well as recruitment and migration defects. These findings reveal a novel post-transcriptional regulatory mechanism of JAK/STAT signalling in the control of epithelial cell invasiveness.