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Multi-generational toxicant exposures show cumulative, inherited health effects

While exposure to a single substance like DDT has been shown to create inherited disease susceptibility, a recent study in animals found exposure to multiple different toxicants across generations can amplify those health problems.

In the study, published in the journal Environmental Epigenetics, an initial generation of pregnant rats was exposed to a common fungicide, then their progeny to jet fuel and the following generation to DDT. When those rats were then bred out to a fifth unexposed generation, the incidence of obesity as well as kidney and prostate diseases in those animals were compounded, rising by as much as 70%.

Researchers also found that their epigenetics, molecular processes independent of DNA that influence gene expression, were also greatly altered.

“We looked at multiple-generation exposures because these types of things are going on routinely, and previous research has only looked at single exposures,” said Michael Skinner, a WSU biology professor and the study’s corresponding author. “We found that if multiple generations get different exposures, then eventually there’s an amplification or compounded effect on some diseases.”

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Tasmanian devil die-off is shifting another predator’s genetics

Devil population crashes caused by contagious tumours have knock-on effects elsewhere in the food chain.

Declining numbers of the endangered Tasmanian devil (Sarcophilus harrisii) are affecting the evolutionary genetics of a small predator, the spotted-tailed quoll (Dasyurus maculatus), according to a study published today in Nature Ecology & Evolution1.

The findings fit with what scientists would expect — typically, when a top predator’s population dwindles, smaller predators increase in number because there are more resources available and less competition.

But little is known about what the effect of a top predator’s decline is on the evolutionary genetics of other species in the food web, says study co-author Andrew Storfer, an evolutionary geneticist at Washington State University in Pullman. “This is one of the first studies to demonstrate that.”

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Even hibernating grizzly bears have a circadian rhythm

There is a pattern to when we wake up and get tired over a 24-hour period, scientists call it the circadian rhythm. Most other animals experience it too.

As winter arrives with its shorter days, grizzly and black bears begin their long naps, called hibernation. During this time bears will still move about a bit, but they don’t eat while hibernating.

Scientists at Washington State University were curious how grizzly bears’ circadian rhythms are affected during hibernation and conducted a study. What they found was although the animals are much less active, the energy their bodies produce still grows and fades over the course of a day as if they were awake, but at a much lower level.

Co-authors on the study include WSU graduate student and first author Ellery Vincent as well as Blair Perry (biological sciences) and Charles Robbins (environment and biological sciences), and Joanna Kelley of University of California, Santa Cruz. This research received support from the National Science Foundation and the Bear Research and Conservation Endowment at WSU.

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Obesity may be caused by ancestors’ exposure to toxic chemicals

Decades ago, someone’s grandmother was exposed to a toxic pesticide that was later banned. A Washington State University professor’s research suggests that person’s grandchild may be suffering the consequences of that environmental exposure.

The inheritance that WSU epigeneticist Michael Skinner studies does not come from genes – those are set in stone after birth. But epigenetics, the way those genes express themselves, do change throughout a person’s life and can also be passed down through the generations.

Skinner suggests that today’s high rates of obesity could be linked to epigenetics rather than just diet and exercise.

Though each cell in the body has an identical DNA sequence, the form and function of cells are often quite different. That is because different epigenetic processes can “turn on and turn off” different cells, according to Skinner.

“Disease we now know primarily comes from an abnormal epigenetics, which is causing an abnormal set of genes to turn on or off and gives genes an abnormal function,” he said.

Unlike DNA, the body’s epigenetics can change throughout their life – largely based on environmental factors. That’s how exposure to a chemical can cause disease decades later.

Over his decades of research, Skinner’s contribution to the field of epigenetics has been the discovery that epigenetics is inherited just like the genes themselves.

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New Method Aims to Curb Disease Spread in Animal Trade

A new article published in the journal Methods in Ecology and Evolution by Morris Animal Foundation-funded researchers describes a simplified method to detect a deadly fungus killing European salamanders. The ability to rapidly find the fungus is significant as the disease, although not detected in the U.S., could impact the millions of amphibians and salamanders annually imported.

The fungal pathogen Batrachochytrium salamandrivorans, or Bsal, threatens salamander diversity. Initially identified in northern Europe, evidence suggests it was introduced from Southeast Asia via the pet trade.

“The impacts of Bsal in Europe have been idiosyncratic but include some of the most severe population declines we have witnessed,” said Jesse Brunner, the study’s principal investigator and associate professor at Washington State University. “A large, diverse group of researchers, government biologists, and amphibian lovers in the pet trade are working hard to avoid such devastating impacts.”

Despite a temporary U.S. ban on importing about 200 salamander species, Brunner noted the researchers’ focus is on preparing for potential arrivals and safeguarding amphibians. To address that concern, the research team developed a noninvasive method to quickly detect Bsal in shipments and captive settings, surpassing the conventional individual animal infection determination — this new method tests environmental DNA for Bsal DNA to assess the pathogen’s prevalence.

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