Inheritance of protection from osmotic stress

Exposure of mother worms to mild osmotic stress induces gene expression changes in offspring that protect them from strong osmotic stress. Inheritance of protection is now shown to depend on altered insulin-like signalling in the maternal germline, which confers protection through increased expression of zygotic gpdh-2, a rate-limiting enzyme in glycerol biosynthesis

Understanding 'non-genetic' inheritance : insights from molecular-evolutionary crosstalk

The idea for this paper was initially proposed by I.A.-K. and was further developed by all authors in a workshop generously funded by grant No 789240 from the European Research Council (ERC) to F.J.W. S.E.S. acknowledges support from Wesleyan University and The John Templeton Foundation.Understanding the evolutionary and ecological roles of 'non-genetic' inheritance (NGI) is daunting due to the complexity and diversity of epigenetic mechanisms. We draw on insights from molecular and evolutionary biology perspectives to identify three general features of 'non-genetic' inheritance systems: (i) they are functionally interdependent with, rather than separate from, DNA sequence; (ii) precise mechanisms vary phylogenetically and operationally; and (iii) epigenetic elements are probabilistic, interactive regulatory factors and not deterministic 'epialleles' with defined genomic locations and effects. We discuss each of these features and offer recommendations for future empirical and theoretical research that implements a unifying inherited gene regulation (IGR) approach to studies of 'non-genetic' inheritance.Publisher PDFPeer reviewe

The Barker hypothesis

The Barker hypothesis proposed that adverse nutrition in early life, including prenatally as measured by birth weight, increased susceptibility to the metabolic syndrome which includes obesity, diabetes, insulin insensitivity, hypertension, and hyperlipidemia and complications that include coronary heart disease and stroke. Periods of rapid postnatal growth associated with high-energy intake seem to be risk factors, along with a high-energy western diet. Theories proposing the mechanism of this association include the thrifty gene, bet-hedging, fetal predictive adaptive response, and drifty phenotype hypotheses. The cause of metabolic syndrome is likely to be multifactorial, with many nuclear DNA and cellular RNA sequences acting in concert with environmental influences. Epidemiological data in humans and experimental data indicate that transgenerational epigenetic inheritance is a possible mechanism where a history of starvation or deprivation during early life is seen in a grandparent and transgenerational effects are seen in their grandchildren. It remains to be seen whether this is mediated by heritable RNA sequences, or by acquired, possibly mosaic mutations in DNA coding for example for regulatory RNAs. Recent research has raised the possibility that the nature and quantity of gastrointestinal microorganisms (microbiota) can be modified by diet and conversely can modify an animal's metabolic program. As the microbiota is inherited largely from the mother, modification of her nutrition, health before and during pregnancy, and mode of delivery could influence the child's microbiota, introducing further potential avenues to improve the prevention, reduction of complications, and treatment of malnutrition and metabolic syndrome