Abstract
Adult stem cells are essential for the proper function of many tissues, yet the mechanisms that maintain the proper identity and regulate proliferative capacity in stem cell lineages are not well understood. Polycomb group (PcG) proteins are transcriptional repressors that have recently emerged as important regulators of stem cell maintenance and differentiation. Here we describe the role of Polycomb Repressive Complex 1 (PRC1) genes Posterior sex combs (Psc) and Suppressor of zeste two (Su(z)2) in restricting the proliferation and maintaining the identity of the Cyst Stem Cell (CySC) lineage in the Drosophila testis. In contrast, Psc and Su(z)2 seem to be dispensable for both germline stem cell (GSC) maintenance and germ cell development. We show that loss of Psc and Su(z)2 function in the CySC lineage results in the formation of aggregates of mutant cells that proliferate abnormally, and display abnormal somatic identity correlated with derepression of the Hox gene Abdominal-B. Furthermore, we show that tumorigenesis in the CySC lineage interferes non-cell autonomously with maintenance of GSCs most likely by displacing them from their niche.
Highlights
Many adult tissues such as blood, skin, and the epithelial lining of the intestine and colon, require a constant supply of newly formed cells produced by the differentiated progeny of adult stem cells
We show that Posterior sex combs (Psc) and Su(z)2 act redundantly to maintain proper identity of the Cyst Stem Cell (CySC) lineage by repressing expression of Abd-B, while Psc and Su(z)2 appear to be dispensable in the germline stem cell (GSC) lineage
Psc and Su(z)2 are functionally redundant and required cell autonomously in the CySC but not the GSC lineage Loss of both Psc and Su(z)2 function in the CySC lineage resulted in formation of an abnormal aggregate of mutant cells at the tip of the testis (Fig. 1A–A’, dotted line) not seen in wild-type controls (Fig. 1B–B’)
Summary
Many adult tissues such as blood, skin, and the epithelial lining of the intestine and colon, require a constant supply of newly formed cells produced by the differentiated progeny of adult stem cells. The mechanisms that regulate and maintain cell identity and fate in adult stem cell lineages are crucial for long-term tissue maintenance and repair. Defects in the mechanisms that regulate stem cell self-renewal versus differentiation and maintain such fate decisions may contribute to tumorigenesis, as many human cancers arise in adult stem cell lineages [1]. Polycomb Group (PcG) proteins have been shown to play an important role in regulating cell fate and stem cell function, and their misregulation may lead to changes in the identity of a stem cell lineage or even cancer [2]. PRC1 members Mel and BMI-1, homologues of Psc and Su(z), play an important role in adult stem cell lineages
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