A Wnt11 and Dishevelled signaling pathway acts prior to injury to control wound polarization for the onset of planarian regeneration.

Regeneration is initiated by wounding, but it is unclear how injury-induced signals precisely convey the identity of the tissues requiring replacement. In the planarian Schmidtea mediterranea, the first event in head regeneration is the asymmetric activation of the Wnt inhibitor notum in longitudinal body-wall muscle cells, preferentially at anterior-facing versus posterior-facing wound sites. However, the mechanism driving this early symmetry-breaking event is unknown.

Noncanonical NF-κB factor p100/p52 regulates homologous recombination and modulates sensitivity to DNA-damaging therapy.

Homologous recombination (HR) serves multiple roles in DNA repair that are essential for maintaining genomic stability, including double-strand DNA break (DSB) repair. The central HR protein, RAD51, is frequently overexpressed in human malignancies, thereby elevating HR proficiency and promoting resistance to DNA-damaging therapies. Here, we find that the non-canonical NF-κB factors p100/52, but not RelB, control the expression of RAD51 in various human cancer subtypes.

Src acts with WNT/FGFRL signaling to pattern the planarian anteroposterior axis.

Tissue identity determination is crucial for regeneration, and the planarian anteroposterior (AP) axis uses positional control genes expressed from body wall muscle to determine body regionalization. Canonical Wnt signaling establishes anterior versus posterior pole identities through notum and wnt1 signaling, and two Wnt/FGFRL signaling pathways control head and trunk domains, but their downstream signaling mechanisms are not fully understood. Here, we identify a planarian Src homolog that restricts head and trunk identities to anterior positions.