Meeting Abstract
We present experiments which characterize beta-catenin’s cellular role during epimorphosis and morphallaxis. Lithium chloride, a GSK-3 inhibitor, was used to prohibit the degradation of β–catenin in two experimental worm populations. The effectiveness of both epimorphosis and morphallaxis were assessed by counting regenerated segments and administering behavioral tests. Worm fragments placed in 14.88mM of lithium chloride (LiCl), wound healed with 90% forming blastemal tissue devoid of segmentation and 0% exhibiting behavioral changes associated with morphallaxis. In the second experiment, worm fragments were treated with 14.88mM LiCl for one week before being placed in 0mM LiCl for a four-week recovery period. During the initial week, segmental regeneration and behavioral changes again were not recorded. However following the recovery period, anterior worm fragments regenerated 6.14+0.1 head segments and posterior worm fragments regenerated 7.5+0.1 head segments. Segmental regeneration was thus not significantly reduced as compared to control populations; even still recovery of behavior was reduced. Posterior worm fragments exhibited posterior behaviors 25% of the time and anterior behaviors 8.3% of the time (n=8). Taken together these data suggest that overexpression of beta-catenin in Lumbriculus results in reduction of functional recovery via morphallaxis but does not significantly effect epimorphosis.
