Halophytes residing in metal-contaminated saltmarsh habitats may employ strategies to enhance fitness of the next generation. We aimed to test the hypothesis that Juncus acutus individuals inhabiting metal-contaminated locations would experience elevated tolerance of offspring to metals compared to plants residing in locations with no metal contamination history. J. acutus seeds (F1 generation) were collected from F0 parent plants residing at eight locations of a contemporary sediment metal gradient (contaminated to uncontaminated) across the coast of NSW, Australia (Hunter river, Lake Macquarie and Georges River). Seeds were exposed in the laboratory to incremental Zn (0.0-1.6 mM) and Pb (0.0-0.50 mM) for nine (9) days, and % germination, germination rate, root elongation and vigour index were assessed for the determination of tolerance. Greater root accumulation (BCF = 1.01) of Zn and subsequent translocation to aerial parts (culm BCF = 0.58 and capsule BCF = 0.85) were exhibited in parents plants, whereas Pb was excluded from roots (BCF = 0.60) and very little translocation to aerial portions of the plant was observed (culm BCF = 0.02 and capsule BCF = 0.05). F1 offspring exhibited tolerance to Zn with EC50 (% germination) significantly correlated with their parents' culm (R2 = 0.93, p = 0.00) and capsule (R2 = 0.57; p = 0.03) Zn. No correlations were observed between offspring Pb tolerance and Pb in parents' plant tissues. Enhanced tolerance to the essential metal Zn may be because Zn is very mobile in the parent plant and seeds experience greater Zn load as a significant portion of sediment Zn reaches capsules (85%). Thus, Zn tolerance in J. acutus seeds is likely attributable to acclimation via maternal transfer of Zn; however, further manipulative experiments are required to disentangle potential acclimation, adaptation or epigenetic effects in explaining the tolerance observed.
Background As a global environmental concern, hypoxia is known to be associated with many biological and physiological impairments in aquatic ecosystems. Previous studies have mainly focused on the effect of hypoxia in adult animals. However, the effect of hypoxia and the underlying mechanism of how hypoxia affects embryonic development of aquatic animals remain unclear. Methodology/Principal Findings In the current study, the effect of hypoxia on primordial germ cell (PGC) migration in zebrafish embryos was investigated. Hypoxic embryos showed PGC migration defect as indicated by the presence of mis-migrated ectopic PGCs. Insulin-like growth factor (IGF) signaling is required for embryonic germ line development. Using real-time PCR, we found that the mRNA expression levels of insulin-like growth factor binding protein (IGFBP-1), an inhibitor of IGF bioactivity, were significantly increased in hypoxic embryos. Morpholino knockdown of IGFBP-1 rescued the PGC migration defect phenotype in hypoxic embryos, suggesting the role of IGFBP-1 in inducing PGC mis-migration. Conclusions/Significance This study provides novel evidence that hypoxia disrupts PGC migration during embryonic development in fish. IGF signaling is shown to be one of the possible mechanisms for the causal link between hypoxia and PGC migration. We propose that hypoxia causes PGC migration defect by inhibiting IGF signaling through the induction of IGFBP-1.