RRC ID 82467
Author Nakamura M, Kyoda T, Yoshida H, Takebayashi-Suzuki K, Koike R, Takahashi E, Moriyama Y, Wlizla M, Horb ME, Suzuki A.
Title Injury-induced cooperation of InhibinβA and JunB is essential for cell proliferation in Xenopus tadpole tail regeneration.
Journal Sci Rep
Abstract In animal species that have the capability of regenerating tissues and limbs, cell proliferation is enhanced after wound healing and is essential for the reconstruction of injured tissue. Although the ability to induce cell proliferation is a common feature of such species, the molecular mechanisms that regulate the transition from wound healing to regenerative cell proliferation remain unclear. Here, we show that upon injury, InhibinβA and JunB cooperatively function for this transition during Xenopus tadpole tail regeneration. We found that the expression of inhibin subunit beta A (inhba) and junB proto-oncogene (junb) is induced by injury-activated TGF-β/Smad and MEK/ERK signaling in regenerating tails. Similarly to junb knockout (KO) tadpoles, inhba KO tadpoles show a delay in tail regeneration, and inhba/junb double KO (DKO) tadpoles exhibit severe impairment of tail regeneration compared with either inhba KO or junb KO tadpoles. Importantly, this impairment is associated with a significant reduction of cell proliferation in regenerating tissue. Moreover, JunB regulates tail regeneration via FGF signaling, while InhibinβA likely acts through different mechanisms. These results demonstrate that the cooperation of injury-induced InhibinβA and JunB is critical for regenerative cell proliferation, which is necessary for re-outgrowth of regenerating Xenopus tadpole tails.
Volume 14(1)
Pages 3679
Published 2024-2-14
DOI 10.1038/s41598-024-54280-w
PII 10.1038/s41598-024-54280-w
PMID 38355764
PMC PMC10867027
MeSH Animals Cell Proliferation Larva / genetics Regeneration* / genetics Signal Transduction* Tail / physiology Xenopus laevis / metabolism
IF 3.998
Resource
Clawed frogs / Newts Xenopus tropicalis