Abstract
Tail resorption in anuran tadpoles is one of the most physically and physiologically notable phenomena in developmental biology. A tail that is over twice as long as the tadpole trunk is absorbed within several days, while concurrently the tadpole's locomotive function is continuously managed during the transition of the driving force from the tail to hindlimbs. Elaborate regulation is necessary to accomplish this locomotive switch. Tadpole's hindlimbs must develop from the limb-bud size to the mature size and the nervous system must be arranged to control movement before the tail is degenerated. The order of the development and growth of hindlimbs and the regression of the tail are regulated by the increasing levels of thyroid hormones (THs), the intracellular metabolism of THs, the expression levels of TH receptors, the expression of several effector genes, and other factors that can modulate TH signaling. The tail degeneration that is induced by the TH surge occurs through two mechanisms, direct TH-responsive cell death (suicide) and cell death caused by the degradation of the extracellular matrix and a loss of cellular anchorage (murder). These pathways lead to the collapse of the notochord, the contraction of surviving slow muscles, and, ultimately, the loss of the tail. In this review, I focus on the differential TH sensitivity of the tail and hindlimbs and the mechanism of tail resorption during Xenopus metamorphosis.