The role of inbreeding depression and mating system in the evolution of heterostyly.

We investigated the role of morph-based differences in the expression of inbreeding depression in loss of the mid-styled morph from populations of tristylous Oxalis alpina. The extent of self-compatibility (SC) of reproductive morphs, the degree of self-fertilization, and the magnitude of inbreeding depression were investigated in three populations of O. alpina differing in their tristylous incompatibility relationships. All three populations exhibited significant inbreeding depression. In two populations with highly modified tristylous incompatibility, manifested as increased reciprocal compatibility between short- and long-styled morphs, substantial SC and self-fertilization of mid-styled morphs were detected, and expected to result in expression of inbreeding depression in the progeny of mid-styled morphs in the natural populations. In contrast, significant self-fertility of the mid-styled morph was absent from the population with typical tristylous incompatibility, and no self-fertilization could be detected. Although self-fertilization and expression of inbreeding depression should result in selection against the mid-styled morph in the later stages of the transition from tristyly to distyly, in O. alpina selection against the mid-styled morph in the early phases of the evolution of distyly is likely due to genic selection against mid-alleles associated with modified tristylous incompatibility, rather than expression of inbreeding depression.

Short-term molecular-level effects of silver nanoparticle exposure on the earthworm, Eisenia fetida.

Short-term changes in levels of expression of nine stress response genes and oxidative damage of proteins were examined in Eisenia fetida exposed to polyvinylpyrrolidone (PVP) coated Ag nanoparticles (Ag-NP) and AgNO(3) in natural soils. The responses varied significantly among days with the highest number of significant changes occurring on day three. Similarity in gene expression patterns between Ag-NPs and AgNO(3) and significant relationships of expression of CAT and HSP70 with Ag soil concentration suggest similarity in toxicity mechanisms of Ag ions and NPs. Significant increases in the levels of protein carbonyls on day three of the exposure to both ions and Ag-NPs indicate that both treatments induced oxidative stress. Our results suggest that Ag ions drive short term toxicity of Ag-NPs in E. fetida. However, given that <15% of Ag in the NPs was oxidized in these soils, dissolution of Ag-NPs is likely to occur after or during their uptake.

Toxicogenomic responses of the model organism Caenorhabditis elegans to gold nanoparticles.

We used Au nanoparticles (Au-NPs) as a model for studying particle-specific effects of manufactured nanomaterials (MNMs) by examining the toxicogenomic responses in a model soil organism, Caenorhabditis elegans . Global genome expression for nematodes exposed to 4-nm citrate-coated Au-NPs at the LC(10) level (5.9 mg·L(-1)) revealed significant differential expression of 797 genes. The levels of expression for five genes (apl-1, dyn-1, act-5, abu-11, and hsp-4) were confirmed independently with qRT-PCR. Seven common biological pathways associated with 38 of these genes were identified. Up-regulation of 26 pqn/abu genes from noncanonical unfolded protein response (UPR) pathway and molecular chaperones (hsp-16.1, hsp-70, hsp-3, and hsp-4) were observed and are likely indicative of endoplasmic reticulum stress. Significant increase in sensitivity to Au-NPs in a mutant from noncanonical UPR (pqn-5) suggests possible involvement of the genes from this pathway in a protective mechanism against Au-NPs. Significant responses to Au-NPs in endocytosis mutants (chc-1 and rme-2) provide evidence for endocytosis pathway being induced by Au-NPs. These results demonstrate that Au-NPs are bioavailable and cause adverse effects to C. elegans by activating both general and specific biological pathways. The experiments with mutants further support involvement of several of these pathways in Au-NP toxicity and/or detoxification.