Habitat-related genetic substructuring in a marine snail (Littorina fabalis) involving a tight link between an allozyme and a DNA locus

Metapopulation structure and genetic differentiation among subpopulations will be tightly related to patterns and processes of local adaptation and microevolution. Understanding the mechanisms behind genetic substructuring will aid in the interpretation of species' ecological performances and strategies. The marine gastropod Littorina fabalis occurs in two size morphs – a small and a large – found in microhabitats of different wave exposure, but overlapping in distribution where wave exposure is intermediate. Earlier studies have found substantial genetic differentiation linked to morph in one allozyme locus (arginine kinase), while 29 other allozyme loci reveal no or minute differences between morphs. Here we add new results showing DNA variation in a RAPD marker being tightly linked to the allozyme variation. Indeed, 97% of the snails homozygotic for one of the Ark alleles had a unique DNA band, while 89% of the snails homozygotic for the other Ark allele lacked the marker. We discuss alternative hypotheses explaining the genetic substructure and suggest that the linkage of size, allozyme and DNA traits might be due to a paracentric chromosomal inversion involving loci coding for these traits. A genetic linkage of traits might promote microhabitat specialization of this species, and such a chromosomal transformation may therefore be adaptive.  © 2004 The Linnean Society of London, Biological Journal of the Linnean Society , 2004, 81 , 301–306.     

Lectin histochemistry for detecting cadmium-induced changes in the glycosylation pattern of rat placenta

Cadmium (Cd) is an industrial and environmental pollutant that produces toxic effects on gametogenesis, pre- and post-implantation embryos, and the placenta. Because the effects of acute Cd intoxication on the placenta are not well understood, we investigated changes in its glycosylated components in Cd treated dams at days 4, 7, 10 and 15 of gestation using lectin histochemistry. CdCl₂ was administered to pregnant rats; control animals received sterile normal saline. Placentas were processed for DBA, Con A, SBA, PNA, UEA-I, RCA-I and WGA lectin histochemistry to evaluate changes in the carbohydrate pattern of the placenta that might modify cell interactions and contribute to embryonic alterations. Lectin binding was analyzed in the yolk sac; trophoblast giant cells; trophoblast I, II and III; spongiotrophoblast cells and endovascular trophoblast cells in the chorioallantoic placenta. Our lectin binding patterns showed that Cd caused alteration of SBA and DBA labeling of trophoblast-derived cells, which suggested increased expressions of α and β GalNAc. Cd also caused decreased UEA-1 binding affinity, which indicated fewer α-L-Fuc residues in placentas of Cd treated dams. The nonreactivity in trophoblast I of the control placentas incubated with Con-A contrasted with the labeling in placentas of experimental dams, which indicated increased expression of terminal α-D-Man, and α-D-Glc residues. We found that Cd altered the reactivity of placenta to several lectins, which indicated modification of the glycotype presented by the fetal component of the placenta. We report that Cd exerts a deleterious effect on the glycosylation pattern of the placenta.