After amputation or feeding, planarian adult pluripotent stem cells (aPSCs) undergo induced and transient hyperproliferation, which is necessary for regeneration. However, the mechanism behind this phenomenon has been unclear. Now, Kiyokazu Agata, Norito Shibata and colleagues reveal the role of plac8 during planarian regeneration. Using asexual fission as a measure of cell proliferation, the authors show that RNAi knockdown of plac8 increases the number of fission events, and thus proliferation, after feeding. In situ hybridisation, immunostaining and qPCR experiments show that plac8 is expressed by most piwi+ aPSCs and negatively correlates with hyperproliferation after feeding and amputation. Spatially, plac8 expression levels are reduced in regions proximal to the blastema during the early stages of regeneration, suggesting that plac8 must be repressed for aPSC proliferation. Indeed, plac8 knockdown increases expression of proliferation markers in aPSCs. Small-molecule inhibition experiments reveal that ERK signalling induces hyperproliferation following amputation by repressing plac8 expression via activation of JNK signalling. Furthermore, JNK signalling inhibition prevents regeneration and cell differentiation, which can be rescued by knockdown of plac8. Together, these data indicate that repression of a single gene, plac8, is sufficient to activate almost all aPSCs to proliferate and differentiate during regeneration.
Planarian plac8 and pluripotent cell proliferation
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Planarian plac8 and pluripotent cell proliferation. Development 1 February 2022; 149 (3): e149_e0301. doi:
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