Discipline: Biological Sciences
Subcategory: Cell and Molecular Biology
Sirai Ramirez - William Paterson University
Co-Author(s): Jaishri Menon and Adonis Rivie, William Paterson University, Wayne, NJ
During metamorphosis, the anuran body changes dramatically to adapt from the aquatic to terrestrial habitat. Larval specific organ/tissue such as the tail completely degenerates by several different mechanisms including those triggered by reactive oxygen species (ROS). Presently we have carried out in situ staining for ROS and mitochondria, peroxisomes, calcium as well as mitochondrial permeability transition pore (MPTP) to finely accentuate their individual roles during the different stages of metamorphosis in tadpoles, Xenopus laevis. During early stages of metamorphosis, there is moderate production of ROS in tail; but prior to and during tail regression, a significant increase in ROS was noted. However, there was no double immunolocalization for ROS and mitochondria indicating that mitochondria are not the source of ROS production. Tail epidermis shows significant increase in peroxisomal density as metamorphosis progressed. Progressive condensation of nuclei from the tip of the tail towards the body also corresponded with a reverse gradient for peroxisome localization. Ventral fin showed signs of cell death before the dorsal fin as wedges of cell death overlapped with ROS localization and peroxisomal staining. We conclude that ROS responsible for cell death in regressing tail, is partly derived from peroxisomes and they seem to be ubiquitous organelles playing a key role in both the production and scavenging of ROS during. Our results on in situ staining for calcium as well as MPTP assay showed an increased expression of these parameters as metamorphosis progressed. Ca2+ signaling has long been known to be critically involved in both the initiation and effectuation of cell death. Oxidative stress accompanied by calcium overload leads to permeability pores of mitochondria to open as tail regression begins. Mitochondrial dysfunction is probably a consequence of calcium overload. Interrelationship between cellular organelles and mechanisms involved in tail regression are discussed.
Funder Acknowledgement(s): This work is partly supported by the National Science Foundation under Grant Number 1040108. Funding was provided by GS-LSAMP of William Paterson University.
Faculty Advisor: Jaishri Menon,