Abstract
Germline stem cell (GSC) self-renewal and differentiation are required for the sustained production of gametes. GSC differentiation in Drosophila oogenesis requires expression of the histone methyltransferase dSETDB1 by the somatic niche, however its function in this process is unknown. Here, we show that dSETDB1 is required for the expression of a Wnt ligand, Drosophila Wingless type mouse mammary virus integration site number 4 (dWnt4) in the somatic niche. dWnt4 signaling acts on the somatic niche cells to facilitate their encapsulation of the GSC daughter, which serves as a differentiation cue. dSETDB1 is known to repress transposable elements (TEs) to maintain genome integrity. Unexpectedly, we found that independent upregulation of TEs also downregulated dWnt4, leading to GSC differentiation defects. This suggests that dWnt4 expression is sensitive to the presence of TEs. Together our results reveal a chromatin-transposon-Wnt signaling axis that regulates stem cell fate.
Highlights
Drosophila female germline stem cells (GSCs) are an excellent tractable model system to study the mechanisms that regulate stem cell division and differentiation [1,2,3]
We study the ovaries of the female Drosophila, whose stem cell population gives rise to gametes
The tissue from which these gametes arise is surrounded by somatic cells, which provide signaling cues required for proper self-renewal and differentiation
Summary
Drosophila female germline stem cells (GSCs) are an excellent tractable model system to study the mechanisms that regulate stem cell division and differentiation [1,2,3]. The CB turns on a differentiation factor, bag of marbles (bam) that is both necessary and sufficient to drive differentiation into a sixteen-cell cyst (Fig 1A) [4,5]. One of these sixteen cells becomes an oocyte, while the other fifteen cells become nurse cells. Two extrinsic factors regulating GSC self-renewal are structural support and Decapentaplegic (Dpp) signaling provided by the terminal filament, cap cells and escort cells located proximally in the somatic niche (Fig 1A) [6,7]. The terminal filament and cap cells provide signaling for GSC self-renewal, while the escort cells physically enclose CBs, allowing for their proper differentiation (Fig 1A) [8,9]. Signaling pathways that regulate escort cell encapsulation, thereby promoting GSC differentiation, have not been fully elucidated
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