Stocking of captive-bred fish can cause long-term population decline and gene pool replacement: predictions from a population dynamics model incorporating density-dependent mortality

Releasing captive-bred fish into natural environments (stocking) is common in fisheries worldwide. Although stocking is believed to have a positive effect on fish abundance over the short term, little is known about the long-term consequences of recurrent stocking and its influence on natural populations. In fact, there are growing concerns that genetically maladapted captive-bred fish can eventually reduce the abundance of natural population. In this study, we develop a simple model to quantitatively investigate the condition under which recurrent stocking has long-term effects on the natural population. Using a population dynamics model that takes into account a density-dependent recruitment, a gene responsible for the fitness difference between wild and captive-bred fish, and hybridization between them, we show that there is little or no contribution of recurrent stocking to the stock enhancement without a replacement of the wild gene pool by the captive-bred gene pool. The model further predicted that stocking of an intermediate level causes a reduction, rather than enhancement, of population size over the long term. The population decline due to stocking was attributed to the fitness disadvantage of captive-bred fish and strong overcompensation at recruitment stage. These results suggest that it would be difficult to simultaneously attain population size recovery and conservation of the local gene pool when captive-bred fish have fitness disadvantage in the wild, although caution is needed when applying the predictions from the simplified model to a specific species or population.

Divergence along a steep ecological gradient in lake whitefish (Coregonus sp.)

To understand mechanisms structuring diversity in young adaptive radiations, quantitative and unbiased information about genetic and phenotypic diversity is much needed. Here, we present the first in-depth investigation of whitefish diversity in a Swiss lake, with continuous spawning habitat sampling in both time and space. Our results show a clear cline like pattern in genetics and morphology of populations sampled along an ecological depth gradient in Lake Neuchâtel. Divergent natural selection appears to be involved in shaping this cline given that trait specific P(ST)-values are significantly higher than F(ST)-values when comparing populations caught at different depths. These differences also tend to increase with increasing differences in depth, indicating adaptive divergence along a depth gradient, which persists despite considerable gene flow between adjacent demes. It however remains unclear, whether the observed pattern is a result of currently stable selection-gene flow balance, incipient speciation, or reverse speciation due to anthropogenic habitat alteration causing two formerly divergent species to collapse into a single gene pool.

In vitro selection of Haemonchus contortus for benzimidazole resistance reveals a mutation at amino acid 198 of beta-tubulin

Benzimidazoles were the first broad-spectrum anthelmintics and are still in use today against gastro-intestinal nematodes of ruminants such as Haemonchus contortus. Benzimidazoles block the polymerization of nematode microtubules. However, their efficacy is jeopardized by the spread of drug-resistant parasites that carry point mutations in beta-tubulin. Here we use a novel in vitro selection-in vivo propagation protocol to breed drug-resistant H. contortus. After 8 generations of selection with thiabendazole an in vitro resistance factor of 1000 was reached that was also relevant in vivo in infected sheep. The same procedure carried out with ivermectin produced only a moderate resistance phenotype that was not apparent in sheep. Cloning and sequencing of the beta-tubulin genes from the thiabendazole-resistant H. contortus mutants revealed all of the isotype 1 alleles, and part of the isotype 2 alleles, to carry the mutation glutamate(198) to alanine (E198A). An allele-specific PCR was developed, which may be helpful in monitoring the prevalence of alanine(198) encoding alleles in the beta-tubulin isotype 1 gene pool of H. contortus in the field.

Evidence for a retroviral insertion in TRPM1 as the cause of congenital stationary night blindness and leopard complex spotting in the horse.

Leopard complex spotting is a group of white spotting patterns in horses caused by an incompletely dominant gene (LP) where homozygotes (LP/LP) are also affected with congenital stationary night blindness. Previous studies implicated Transient Receptor Potential Cation Channel, Subfamily M, Member 1 (TRPM1) as the best candidate gene for both CSNB and LP. RNA-Seq data pinpointed a 1378 bp insertion in intron 1 of TRPM1 as the potential cause. This insertion, a long terminal repeat (LTR) of an endogenous retrovirus, was completely associated with LP, testing 511 horses (χ(2)=1022.00, p<0.0005), and CSNB, testing 43 horses (χ(2)=43, p<0.0005). The LTR was shown to disrupt TRPM1 transcription by premature poly-adenylation. Furthermore, while deleterious transposable element insertions should be quickly selected against the identification of this insertion in three ancient DNA samples suggests it has been maintained in the horse gene pool for at least 17,000 years. This study represents the first description of an LTR insertion being associated with both a pigmentation phenotype and an eye disorder.

Ecosystem size matters: The dimensionality of intralacustrine diversification in Icelandic stickleback is predicted by lake size

Cases of evolutionary diversification can be characterized along a continuum from weak to strong genetic and phenotypic differentiation. Several factors may facilitate or constrain the differentiation process. Comparative analyses of replicates of the same taxon at different stages of differentiation can be useful to identify these factors. We estimated the number of distinct phenotypic groups in threespine stickleback populations from nine lakes in Iceland and in one marine population. Using the inferred number of phenotypic groups in each lake, genetic divergence from the marine population, and physical lake and landscape variables, we tested if ecosystem size, approximated by lake size and depth, or isolation from the ancestral marine gene pool predict the occurrence and the extent of phenotypic and genetic diversification within lakes. We find intralacustrine phenotypic diversification to be the rule rather than the exception, occurring in all but the youngest lake population and being manifest in ecologically important phenotypic traits. Neutral genetic data further indicates non-random mating in four out of nine studied lakes, and restricted gene flow between sympatric phenotypic groups in two. Although neither the phenotypic variation nor the number of intralacustrine phenotypic groups were associated with any of our environmental variables, the number of phenotypic traits that were differentiated was significantly positively related to lake size, and evidence for restricted gene flow between sympatric phenotypic groups was only found in the largest lakes where trait specific phenotypic differentiation was highest.

Cardiac sodium channel NaV1.5 distribution in myocytes via interacting proteins: the multiple pool model

The cardiac sodium current (INa) is responsible for the rapid depolarization of cardiac cells, thus allowing for their contraction. It is also involved in regulating the duration of the cardiac action potential (AP) and propagation of the impulse throughout the myocardium. Cardiac INa is generated by the voltage-gated Na(+) channel, NaV1.5, a 2016-residue protein which forms the pore of the channel. Over the past years, hundreds of mutations in SCN5A, the human gene coding for NaV1.5, have been linked to many cardiac electrical disorders, including the congenital and acquired long QT syndrome, Brugada syndrome, conduction slowing, sick sinus syndrome, atrial fibrillation, and dilated cardiomyopathy. Similar to many membrane proteins, NaV1.5 has been found to be regulated by several interacting proteins. In some cases, these different proteins, which reside in distinct membrane compartments (i.e. lateral membrane vs. intercalated disks), have been shown to interact with the same regulatory domain of NaV1.5, thus suggesting that several pools of NaV1.5 channels may co-exist in cardiac cells. The aim of this review article is to summarize the recent works that demonstrate its interaction with regulatory proteins and illustrate the model that the sodium channel NaV1.5 resides in distinct and different pools in cardiac cells. This article is part of a Special Issue entitled: Cardiomyocyte Biology: Cardiac Pathways of Differentiation, Metabolism and Contraction.

Neuronal differentiation of human mesenchymal stem cells: changes in the expression of the Alzheimer's disease-related gene seladin-1

Seladin-1 (SELective Alzheimer's Disease INdicator-1) is an anti-apoptotic gene, which is down-regulated in brain regions affected by Alzheimer's disease (AD). In addition, seladin-1 catalyzes the conversion of desmosterol into cholesterol. Disruption of cholesterol homeostasis in neurons may increase cell susceptibility to toxic agents. Because the hippocampus and the subventricular zone, which are affected in AD, are the unique regions containing stem cells with neurogenic potential in the adult brain, it might be hypothesized that this multipotent cell compartment is the predominant source of seladin-1 in normal brain. In the present study, we isolated and characterized human mesenchymal stem cells (hMSC) as a model of cells with the ability to differentiate into neurons. hMSC were then differentiated toward a neuronal phenotype (hMSC-n). These cells were thoroughly characterized and proved to be neurons, as assessed by molecular and electrophysiological evaluation. Seladin-1 expression was determined and found to be significantly reduced in hMSC-n compared to undifferentiated cells. Accordingly, the total content of cholesterol was decreased after differentiation. These original results demonstrate for the first time that seladin-1 is abundantly expressed by stem cells and appear to suggest that reduced expression in AD might be due to an altered pool of multipotent cells.