Wnt/β-catenin signaling promotes posterior axial regeneration in non-regenerative tissue of the annelid Capitella teleta

To rescue regeneration, the mechanisms underlying regeneration failure must be identified and overcome. In the annelid Capitella teleta , a transverse cut triggers asymmetric responses across the amputation plane: head fragments regenerate the tail, but tail fragments do not regenerate. We compare regeneration of head fragments (successful regeneration) to that of tail fragments (unsuccessful regeneration) using cell proliferation assays, immunolabeling, and in situ hybridization. Surprisingly, following amputation, a dynamic response of the nervous system occurs in the non-regenerating tail fragments of C. teleta that has not previously been described in annelids. Wnt/β-catenin signaling plays a conserved role in patterning the primary axis of some bilaterians during regeneration, but this role has never been demonstrated in annelids. Wnt/β-catenin pathway components are expressed in the blastema of head fragments but not at the cut site of tail fragments in C. teleta . Experimental activation of Wnt/β-catenin signaling following amputation of tail fragments (24 – 72 hr post amputation) induces expression of stem cell markers, increases cell division at the wound site, and produces differentiated muscle and hindgut. Furthermore, activation of Wnt/β-catenin signaling induces ectopic posterior identity at the amputation site, as it does in other bilaterians. Inhibition of Wnt/β-catenin signaling does not rescue head regeneration. Our results indicate that C. teleta tail fragments have latent regenerative potential that is activated by Wnt/β-catenin signaling. However, the incomplete regenerative response suggests that additional cell signaling pathways are required for this complex process. Comparing tissues with different regenerative abilities elucidates the mechanisms underlying regeneration regulation, thereby enabling the prospect of rescuing or increasing regeneration ability in regeneration-deficient tissues.