Abstract
Neoblasts are an abundant, heterogeneous population of adult stem cells (ASCs) that facilitate the maintenance of planarian tissues and organs, providing a powerful system to study ASC self-renewal and differentiation dynamics. It is unknown how the collective output of neoblasts transit through differentiation pathways to produce specific cell types. The planarian epidermis is a simple tissue that undergoes rapid turnover. We found that as epidermal progeny differentiate, they progress through multiple spatiotemporal transition states with distinct gene expression profiles. We also identified a conserved early growth response family transcription factor, egr-5, that is essential for epidermal differentiation. Disruption of epidermal integrity by egr-5 RNAi triggers a global stress response that induces the proliferation of neoblasts and the concomitant expansion of not only epidermal, but also multiple progenitor cell populations. Our results further establish the planarian epidermis as a novel paradigm to uncover the molecular mechanisms regulating ASC specification in vivo.
Highlights
Adult stem cells (ASCs) are tissue-specific cells with the capacity to self-renew and differentiate to continually replace cells lost to normal physiological turnover or injury
The prog-1+ and AGAT-1+ postmitotic cell populations constituting the first neoblast lineage described in planarians (Eisenhoffer et al, 2008) have been widely used as an assay for neoblast differentiation (Fraguas et al, 2011; Pearson and Sanchez Alvarado, 2010; Scimone et al, 2010; Wagner et al, 2012)
We provide further evidence that the planarian epidermis is an experimentally tractable system to study the complex dynamics and hierarchical transitions that are likely to occur during adult lineage specification and progression
Summary
Adult stem cells (ASCs) are tissue-specific cells with the capacity to self-renew and differentiate to continually replace cells lost to normal physiological turnover or injury. Excessive stem cell divisions can lead to tumorigenesis (Visvader and Lindeman, 2012), while a loss in proliferation capacity can contribute to premature aging (Gopinath and Rando, 2008). Understanding the cellular and molecular mechanisms that regulate the balance between stem cell proliferation, differentiation, and cell death will provide fundamental insights into tissue maintenance and repair. It will illuminate the molecular basis of tissue dysfunction, including disease progression and aging
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