فرورفتگی سلولهای بنیادی نر مگس سرکه
Abstract
1- Introduction
2- Materials and methods
3- Results
4- Discussion
References
Abstract
The Drosophila male stem cell niche is a well characterized structure in which a small cluster of somatic cells send self-renewal signals to neighbouring germ cells. Although the molecular information involved in the stem cell fate have been identified, much less is understand on the mechanisms driving their short-range specific release. Our ultrastructural analysis reveals distinct protrusions of the stem cell plasma membrane that interdigitate with membrane protrusions of the facing hub cells. Some of these protrusions are very elongated and extend into the hub and could correspond to the Mt-Nanotubes. Therefore, the interface between the stem cells and the hub appears more complex than previously reported and the membrane protrusions of the stem cells might represent specialized surface areas involved in the niche-stem cell communication. We also noticed the presence of clathrin-coated vesicles in the germline plasma membrane that might be also involved in delivering information from the hub.
Introduction
One of the best-known stem cell niche systems is restricted to the apical tip of the Drosophila testis. Here, a crown of 8–10 germline stem cells (GSCs) surrounds a cluster of small post-mitotic somatic cells, the hub [1]. The GSCs divide asymmetrically to produce two daughters, one daughter remains attached to the hub and maintains stem cell fate, while the other daughter, the gonialblast, is displaced away and initiates the differentiation program. A pair of somatic cyst stem cells (CySCs) surrounds each GSC and divide asymmetrically to produce a pair of somatic stem cell daughters and two cyst cells that surround the gonialblast. The different fate of the stem cell progeny is ensured by upstream signals that travel within the niche microenvironment triggering stemness or differentiation. In Drosophila, the hub represents the source of two main self-renewal factors, the cytokine-like ligand Unpaired (Upd) and the Bone Morphogenetic Protein ligand Decapentaplegic (Dpp). Upd through its receptor Domeless (Dome) activates the Janus Kinase Transducer and Activator of Transcription (JAK/ STAT) [2] pathway that supports GSC maintenance by promoting the stem cell adhesion to the hub [3]. The Dpp signal that is supplied by both the hub and the CySCs [4] activates the R-Smad transcription factor Mother against Dpp (Mad) that promotes GSC fate by preventing the expression of the specific differentiation gene Bam-of-marbles (Bam) so that Bam is silenced in GSCs but active in gonialblasts [5].