Celeste Kidd and Steven Piantadosi had sued the university over its handling of sexual harassment allegations made against colleague Florian Jaeger.
Oldest hominin DNA sequence; visualizing dyslexia; testing CRISPR; cancer and autoimmunity
December 6, 2013|
MEYER ET AL.Matthias Meyer from the Max Planck Institute for Evolutionary Anthropology and his colleagues have sequenced the oldest hominin DNA to date, generating a nearly complete mitochondrial genome of a human ancestor who lived around 400,000 years ago.
“It’s an incredible breakthrough,” David Reich from Harvard Medical School, who was not involved in the study, told The Scientist. “They managed to get DNA out of a sample that dates back to a time before either modern humans or Neanderthals existed.”
Phylogenetic analyses involving this and other ancient specimens proved puzzling. “Obviously, the origins of Neanderthals and Denisovans are quite complicated, perhaps more than what we would have hoped,” said Meyer. “[Our results] just put a big question mark over all of this.”
BART BOETSPhonetic representations are not compromised in the brains of adults with dyslexia, it turns out. Researchers used advanced neuroimaging techniques to show that the brain’s interpretations of human speech sounds were, by all accounts, normal.
“Even while scanning throughout the whole brain for local regions where the representations may be impaired . . . we could not find a single region with inferior phonetic representations in dyslexics as compared to typical readers,” lead author Bart Boets from Katholieke Universiteit Leuven told The Scientist.
Rather, the researchers found evidence to suggest that the reading disorder arises from a dysfunctional connection between frontal and temporal language areas of the brain that impairs access to otherwise intact phonetic representations.
“This paper, by telling us more about at what level in the brain things break down, can help in directing interventions,” said Guinevere Eden, who directs the Center for the Study of Learning at Georgetown University and was not involved in the work.
JINSONG LITwo separate studies published this week are the first to show that CRISPR can be used to rewrite genetic defects to effectively cure diseases in mice and human stem cells. Jinsong Li from the Shanghai Institute for Biological Sciences applied CRISPR/Cas9-based genome editing techniques to correct a cataract-causing mutation in mice. Working independently, the Hubrecht Institute’s Hans Clevers used the same technique to correct a defect associated with cystic fibrosis in human stem cells.
“What’s significant about this is it’s taking CRISPR to that next step of what it can be used for, and in this case, it’s correcting mutations that cause disease,” said Charles Gersbach, a genomics researcher at Duke University, who was not involved in either study.
WIKIMEDIA, AVMAntony Rosen from Johns Hopkins University and his colleagues this week showed that that antibodies produced by the body to recognize a mutant protein in tumor cells also bind to the protein’s normal counterpart, and can cause damage to healthy tissues. This mechanismis thought to underlie the autoimmune disorder scleroderma.
“The study provides still more evidence that immune regulation and immune surveillance of cancer are important processes,” Tyler Jacks, who is director of the Koch Institute for Integrative Cancer Research at the Massachusetts Institute of Technology and was not involved in the work, told The Scientist.
FLICKR, E3000Different levels of immune chemicals in mouse mothers’ milk can help prepare their pups for future challenges, scientists found this week. “We think TNF [tumor necrosis factor α] could be an environmental sensor. . . . It responds to conditions like stress or food supply,” said Weill Cornell Medical College’s Miklos Toth, who led the study. “It allows the mother to match her offspring’s cognitive performance to the environment she experiences.”
Like mouse milk, human milk contains TNF, along with several other chemokines, but “there is some evidence that this TNF may be biologically inactive because milk contains soluble TNF receptors that inactivate it,” Roberto Garofalo, an immunologist at the University of Texas Medical Branch who was not involved in the work, told The Scientist.
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