Experimental transplantation of the adenohypophysisprimordium into the anura embryo.
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High prevalences of hindlimb deformities were recorded in wild-caught green frogs (Rana clamitans), northern leopard frogs (Rana pipiens), American toads, (Bufo americanus), and bullfrogs (Rana catesbeiana) from agricultural sites exposed to pesticide runoff in the St. Lawrence River Valley of Québec, Canada, between July and September 1992 and 1993. Of 853 metamorphosing anurans examined in 14 farmland habitats, 106 (12%; range 0 to 69%) had severe degrees of ectromelia and ectrodactyly, compared to only two (0.7%; range 0 to 7.7%) of 271 in 12 control sites. However, the variation in the proportion of deformities among sites was too large to conclude that there was a significant difference between control and pesticide-exposed habitats. Clinical signs varied and were characterized by segmental hypoplasia or agenesis of affected limbs. Conspicuous abnormalities interfered with swimming and hopping, and likely constituted a survival handicap. Because of circumstances and the frequency of these malformations in nine distinct habitats, and in three different species from one of our study sites, we propose a teratogenic action of exogenous factors. Despite the fact that many biotic and abiotic agents are potentially harmful to limb development, agricultural contaminants were suspected as primary aggressors. Thus, clinical examination and frequency of deformities in anurans might be an economical screening tool to assess ecosystem health and the presence of environmental contaminants.
Cadherins and N-CAM are Ca++-dependent and Ca++-independent cell adhesion molecules respectively. These molecules play a key role in morphogenesis and histogenesis. We determined the spatiotemporal pattern of N-cadherin and N-CAM-180 kDa expression by immunohistochemistry during development in two South-American anuran species (Bufo arenarum, toad and Hyla nana, frog). Both N-cadherin and N-CAM were not detectable during early developmental stages. Expression of N-cadherin appeared between the inner and the outer ectoderm layers at stages 19-20. At stages 24-25, N-cadherin was expressed in the neural tube and the heart. In early tadpoles, N-cadherin expression increased along with the central nervous system (CNS) morphogenesis, and reached its maximum level at metamorphic climax stage. N-Cadherin expression was not uniformly distributed. At stage 42, olfactory placodes and retina expressed N-cadherin. Contrary to N-CAM, the strongly myelinated cranial nerves were not labeled. N-Cadherin was present in several mesoderm derivatives such as the notochord, heart and skeletal muscle. The non-neural ectoderm and the endoderm were always negative. Expression of N-CAM appeared first in the neural tube at stages 24-25 and the level of expression became uniform from pre-metamorphic to metamorphic climax tadpoles. At this latter stage, a clear N-CAM immunolabeling appeared in the nerve terminals of pharynx and heart. N-Cadherin and N-CAM were found mainly co-expressed in the CNS from early tadpole to metamorphic climax tadpole. Our results show that the expression of N-CAM and N-cadherin is evolutionary conserved. Their increased expression during late developmental stages suggests that N-CAM and N-cadherin are involved in cell contact stabilization during tissue formation.
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