Biologists use sound to identify breeding grounds of endangered whales

Remote acoustic monitoring among endangered whales is the subject of a major article by two doctoral students in The College of Arts and Sciences.

Leanna Matthews and Jessica McCordic, members of the Parks Lab in the Department of Biology, have co-authored "Remote Acoustic Monitoring of North Atlantic Right Whales Reveals Seasonal and Diel Variations in Acoustic Behavior." The article appears in the current issue of PLOS ONE, an inclusive, peer-reviewed, open-access resource from the Public Library of Science in San Francisco.

Susan Parks, assistant professor of biology for whom the lab is named, says the article confirms what many conservationists fear -- that Roseway Basin, a heavily traveled shipping lane, off the coast of Nova Scotia, is a vital habitat area for the endangered North Atlantic right whale.

"Remote acoustic monitoring is an important tool for understanding patterns in animal communication, and studies on the seasonality of context-specific acoustic signals allow inferences to be made about the behavior and habitat use of certain species," says Parks, an expert in behavioral ecology, acoustic communication and marine science. "Our results support the hypothesis that the North Atlantic right whale's breeding season occurs mostly from August to November and that this basin is a widely used habitat area."

More than 30 percent of all right whales use Roseway Basin, part of a larger geological formation called the Scotian Shelf, throughout the year. With only 400-500 in existence, these whales, says Parks, must congregate in the basin to feed and find mates.

Already, the U.S. and Canadian governments have taken steps to redirect shipping traffic, in response to several fatal collisions with right whales.

Matthews, whose research includes animal behavior and physiology, says the object of the article is to determine how and when Roseway Basin is used for male breeding activities.

"Part of the answer lies in a loud 'gunshot' sound, made by the male whale," says Matthews, the article's lead author. "We're not exactly sure what the gunshot is, but we think it may be a male-to-male antagonistic signal or an advertisement to females. … During a two-year period, we used non-invasive acoustic monitoring to analyze gunshots at two locations on the Scotian Shelf. The resultant data has provided tremendous insights into the whales' feeding and mating habits."

Matthews and her team found that gunshot sound production occurred mainly in the autumn and, more often than not, at night. Researchers say this kind of information is essential to not only the individual fitness of each whale, but also the survival of the species, in general.

McCordic, whose research spans animal behavior and communication, says the observed seasonal increase in gunshot sound production is consistent with the current understanding of the right whale breeding season.

"Our results demonstrate that detection of gunshots with remote acoustic monitoring can be a reliable way to track shifts in distribution and changes in acoustic behavior, including possible mating activities," she says, acknowledging David Mellinger, associate professor of marine bioacoustics at Oregon State University, who collected and provided access to the recordings used in the study. "It also provides a better understanding of right whale behavior and what needs to be done with future conservation efforts."

Parks, who assisted with the article, is proud of her students' accomplishments.

"Right whales are increasingly rare, and Leanna's and Jessica's research helps us understand how to better protect them," she says. "By identifying potential breeding areas, we might be able to save this critically endangered species."

Story Source:

The above story is based on materials provided by Syracuse University. Note: Materials may be edited for content and length.

View the original article here

Biologists ID new cancer weakness

Nov. 14, 2013 — About half of all cancer patients have a mutation in a gene called p53, which allows tumors to survive and continue growing even after chemotherapy severely damages their DNA.

A new study from MIT biologists has found that tumor cells with mutated p53 can be made much more vulnerable to chemotherapy by blocking another gene called MK2. In a study of mice, tumors lacking both p53 and MK2 shrank dramatically when treated with the drug cisplatin, while tumors with functional MK2 kept growing after treatment.

The findings suggest that giving cancer patients a combination of a DNA-damaging drug and an MK2 inhibitor could be very effective, says Michael Yaffe, the David H. Koch Professor in Science and senior author of a paper describing the research in the Nov. 14 issue of the journal Cell Reports.

Several drugs that inhibit MK2 are now in clinical trials to treat inflammatory diseases such as arthritis and colitis, but the drugs have never been tested as possible cancer treatments.

"What our study really says is that these drugs could have an entirely new second life, in combination with chemotherapy," says Yaffe, who is a member of MIT's Koch Institute for Integrative Cancer Research. "We're very much hoping it will go into clinical trials" for cancer.

Sandra Morandell, a postdoc at the Koch Institute, is the paper's lead author.

To kill a tumor

P53 is a tumor-suppressor protein that controls cell division. Before cell division begins, p53 checks the cell's DNA and initiates repair, if necessary. If DNA damage is too extensive, p53 forces the cell to undergo programmed cell death, or apoptosis. Tumors that lack p53 can avoid this fate.

"Usually p53 is the main driver of cell death, and if cells lose this pathway they become very resistant to different treatments that cause cell death," Morandell says.

Several years ago, researchers in Yaffe's lab discovered that in cancer cells with mutated p53, the MK2 gene helps counteract the effects of chemotherapy. When cancer cells suffer DNA damage, MK2 puts the brakes on the cell division cycle, giving cells time to repair the damage before dividing.

"Our data suggested if you block the MK2 pathway, tumor cells wouldn't recognize that they had DNA damage and they would keep trying to divide despite having DNA damage, and they would end up committing suicide," Yaffe says.

In the new study, the researchers wanted to see if this would hold true in tumors in living animals, as well as cells grown in a lab dish. To do that, they used a strain of mice that are genetically programmed to develop non-small-cell lung tumors. The researchers further engineered the mice so they could reversibly turn the MK2 gene on or off, allowing them to study tumors with and without MK2 in the same animal.

This new approach allows them, for the first time, to compare different types of tumors in the same mice, where all genetic factors are identical except for MK2 expression.

Using these mice, the researchers found that before treatment, tumors lacking both MK2 and p53 grow faster than tumors that have MK2. This suggests that treating tumors with an MK2 inhibitor alone would actually do more harm than good, possibly increasing the tumor's growth rate by taking the brake off the cell cycle.

However, when these tumors are treated with cisplatin, the tumors lacking MK2 shrink dramatically, while those with MK2 continue growing.

'A nonobvious combination'

The potential combination of cisplatin and MK2 inhibitors is unlike other chemotherapy combinations that have been approved by the Food and Drug Administration, which consist of pairs of drugs that each show benefit on their own. "What we found is a combination that you would never have arrived at otherwise," Yaffe says. "It's a nonobvious combination."

While this study focused on non-small-cell lung tumors, the researchers have gotten similar results in cancer cells grown in the lab from bone, cervical, and ovarian tumors. They are now studying mouse models of colon and ovarian cancer.

View the original article here

2 molecular biologists get $500K medical prize

AppId is over the quota
AppId is over the quota

ALBANY, N.Y. (AP) — Two molecular biologists have been awarded the annual Albany Medical Center Prize in Medicine and Biomedical Research.

James Darnell Jr. and Robert Roeder received the prize during a ceremony Friday and will share $500,000, the largest award in medicine and science in the United States. The two men performed pioneering research on how cells express their genetic information.

Roeder heads the biochemistry and molecular biology lab at The Rockefeller University in New York City, where Darnell is emeritus faculty.

The two winners were announced in March.