Marmosets that glow green

By inserting foreign DNA into the mouse genome to generate transgenic mice, scientists have created models of human disorders from autism to diabetes. For certain diseases, however, mouse models do not fully represent all the characteristics of human disease. As a result, researchers hope to generate transgenic animals that are more closely related to humans. Last year, scientists generated transgenic monkeys that model Huntington's disease (Nature 453, 921–924; 2008), but it is not known whether offspring of such monkeys would also express the transgene.

Now, Erika Sasaki (Central Institute for Experimental Animals, Japan) and her colleagues have reported the generation of transgenic marmosets as the first non-human primates to pass on a foreign gene to their offspring (Nature 459, 523–528; 2009). The research team injected a transgene encoding green fluorescent protein (GFP) into 91 marmoset embryos. They then transferred 80 of these embryos into 50 surrogate female marmosets, resulting in seven pregnancies and five viable offspring. All five of these offspring expressed GFP in various tissues, causing these tissues to glow green under ultraviolet light. Two of the five marmosets expressed GFP in their germ cells, and one fathered a healthy transgenic marmoset.

If these mice could talk

Although mouse models have clarified the workings of some human diseases, we may not have considered that they could teach us about human evolution. But new research suggests that mice may have something to say about this aspect of ourselves as well.

The new work targeted the human transcription factor FOXP2, which has only two amino acids that differ from the chimpanzee version. These amino acid changes are thought to have undergone positive selection in humans because they affected speech and language. Investigating the potential influence of these changes on human evolution is difficult, however, because genetic manipulations of humans and chimpanzees cannot be done; the mouse is the only mammal in which such experiments are possible.

Therefore, Wolfgang Enard (Max-Planck Institute for Evolutionary Anthropology, Leipzig, Germany) and colleagues modified the mouse version of FOXP2 to mimic the amino acid changes that differentiate the human from the chimp versions (Cell 137, 961–971; 2009). Mice expressing the modified FOXP2 were generally healthy, but their vocalizations were different from those of wild-type mice and their exploratory behavior and brain dopamine concentrations were reduced. These results suggest that the modified FOXP2 affected basal ganglia and that changes in these circuits may be important for the evolution of human speech and language.

Calling all white blood cells

Within a short time after a wound is sustained, white blood cells, or leukocytes, flood the wound area, sometimes traveling from relatively long distances. But the signal that calls them to the wound site has, until recently, been a mystery. Now, Phillip Neithammer (Harvard Medical School, Boston, MA), Clemmens Grabber (Dana-Farber Cancer Institute, Boston MA) and colleagues report that hydrogen peroxide is the molecule that makes the call, at least in zebrafish.

The scientists had been investigating methods of detecting reactive oxygen species, a group of molecules that includes hydrogen peroxide. They developed zebrafish embryos carrying a transgene designed to change color in the presence of hydrogen peroxide. After inflicting small wounds to the tail fins of the transgenic zebrafish larvae, they immediately observed hydrogen peroxide at the wound site spreading into adjacent tissue, the concentration decreasing as distance from the wound increased (Nature published online 3 June 2009; doi: 10.1038/nature08119). In further experiments using zebrafish with a mutation that prevented them from creating hydrogen peroxide, no leukocytes were recruited to the wound site, indicating that hydrogen peroxide was the necessary signal.

These results may have implications for human diseases that involve disproportionate numbers of leukocytes, such as asthma.