In metazoans, tissue maintenance and regeneration depend on adult stem cells, which are characterized by their ability to self-renew and generate differentiating progeny in response to the needs of the tissues in which they reside. In the Drosophila testis, germline and somatic stem cells are housed together in a common niche, where they are regulated by local signals, epigenetic mechanisms and systemic factors. These stem cell populations in the Drosophila testis have the unique advantage of being easy to identify and manipulate, and hence much progress has been made in understanding how this niche operates. Here, we summarize recent work on stem cells in the adult Drosophila testis and discuss the remarkable ability of these stem cells to respond to change within the niche.
"The somatic cyst stem cells (CySCs) serve as a component of the niche for the germline stem cells (GSCs). In fact, it is a combination of signals derived from the terminally differentiated hub cells to which CySCs and GSCs are adhered and the CySCs themselves that are necessary for GSC maintenance (de Cuevas and Matunis, 2011; Leatherman and Dinardo, 2008, 2010; Figure 1A). Similar to regulation in the hair follicle niche, the generation of daughter cells by GSCs and CySCs in the testis must be tightly controlled. "
"One of the best characterized niches is found in the Drosophila testis apex, where a cluster of quiescent somatic cells called the hub creates a niche that maintains adjacent germline stem cells (GSCs) and somatic cyst stem cells (CySCs) (Figure 1A) (de Cuevas and Matunis, 2011). GSCs and CySCs divide asymmetrically , producing new stem cells (self-renewal) and daughters that are displaced from the hub and differentiate. "
[Show abstract][Hide abstract] ABSTRACT: Adult stem cells reside in specialized regulatory microenvironments, or niches, where local signals ensure stem cell maintenance. The Drosophila testis contains a well-characterized niche wherein signals from postmitotic hub cells promote maintenance of adjacent germline stem cells and somatic cyst stem cells (CySCs). Hub cells were considered to be terminally differentiated; here, we show that they can give rise to CySCs. Genetic ablation of CySCs triggers hub cells to transiently exit quiescence, delaminate from the hub, and convert into functional CySCs. Ectopic Cyclin D-Cdk4 expression in hub cells is also sufficient to trigger their conversion into CySCs. In both cases, this conversion causes the formation of multiple ectopic niches over time. Therefore, our work provides a model for understanding how oncogenic mutations in quiescent niche cells could promote loss of quiescence, changes in cell fate, and aberrant niche expansion.
"This niche provides signals that regulate GSC self-renewal and differentiation. The SSCs are non-dividing and enclose the GSC daughter cell that will ultimately give rise to sperm or eggs (Fuller and Spradling, 2007; Kirilly and Xie, 2007; Voog and Jones, 2010; de Cuevas and Matunis, 2011). Previous studies suggested the importance of microRNA biogenesis in the maintenance of ovarian stem cells. "
[Show abstract][Hide abstract] ABSTRACT: Follicle-stimulating hormone (FSH) is a master endocrine regulator of mammalian reproductive functions. Hence, it is used to stimulate folliculogenesis in assisted reproductive technologies (ART), both in women and in breeding animals. However, the side effects that hormone administration induces in some instances jeopardize the success of ART. Similarly, the luteinizing hormone (LH) is also of paramount importance in the reproductive function because it regulates steroidogenesis and the LH surge is a pre-requisite to ovulation. Gaining knowledge as extensive as possible on gonadotropin-induced biological responses could certainly lead to precise selection of their effects in vivo by the use of selective agonists at the hormone receptors. Hence, over the years, numerous groups have contributed to decipher the cellular events induced by FSH and LH in their gonadal target cells. Although little is known on the effect of gonadotropins on microRNA expression so far, recent data have highlighted that a microRNA regulatory network is likely to superimpose on the signaling protein network. No doubt that this will dramatically alter our current understanding of the gonadotropin-induced signaling networks. This is the topic of this review to present this additional level of complexity within the gonadotropin signaling network, in the context of recent findings on the microRNA machinery in the gonad.
Frontiers in Cell and Developmental Biology 12/2013; 1:3. DOI:10.3389/fcell.2013.00003
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