SEEING THE RETINA Borrowing a technique that clarifies images from spy satellites, researchers from the University of Rochester have imaged the distribution of cone cells in the human retina (A. Roorda, D.R. Williams, Nature, 397:520-2, Feb. 11, 1999). The three types of cone cells have photopigments that absorb predominantly short (S), middle (M), or long (L) wavelengths, corresponding to blue/violet, green, and red. Color vision works much like a color television--the brain integrates the individual pixels so that we see a rainbow of colors. S cones were known to form a regular mosaic on the retina, but the M and L cones were difficult to distinguish because their photopigments are similar. The military's adaptive optics approach shines light into the eye and a deformable mirror aligns the reflected beams, correcting for distortion from the lens and cornea. The researchers distinguished between M and L cones because each bleaches different incoming wavelengths of light. Results were surprising. "One man had four times the number of L cones than M cones, but his color vision is not that different from the man with a 1:1 ratio," says David Williams, director of Rochester's Center for Visual Science, who did the work with Austin Roorda, an assistant professor of optics at the University of Houston College of Optometry. Plus, the patterns of cone types differed. "It is interesting how well the brain gets around big differences in the relative number and distribution of cone types," Williams adds.
SUNBURNED TRANSPOSONS Ultraviolet (UV) rays cause mutations by damaging DNA, but Virginia Walbot, professor of biological sciences at Stanford University, thinks she's found another mechanism: transposable elements. Transposons are bits of DNA that jump from gene to gene under the control of a transposase enzyme, and in doing so, induce mutations. Walbot discovered that UV reactivates silent transposons in maize, which they studied because 70 percent of its DNA consists of transposons and their silent relics. Walbot exposed pollen containing an inactive transposon called Mutator (Mu) to UV-B radiation, then used that pollen in crosses with plants containing a reporter gene for anthocyanin pigment synthesis (Nature, 397:398-9, Feb. 4, 1999). The reporter gene contains a defective Mu; pigmentation returns if Mu jumps out. Each pollen grain contains two sperm, one of which contributes to the embryo and the other to nutritive storage tissue in the kernel. A reactivated Mu transposase in a sperm that contributed to the storage tissue would occasionally cause the Mu element in the reporter gene to excise. Pigment spotting signaled such events in seven of 19 progeny ears. When Mu reactivated in the other sperm, seedlings had a functioning transposase gene and made spotted kernels after they grew and flowered.
--Barry A. Palevitz
TELLTALE TANGLES The first inklings of Alzheimer's disease are notoriously difficult to detect, but results from a 15-year study confirm what many researchers have long suspected--telltale protein plaques and tangles that choke the memory-making hippocampus develop before a person notices forgetfulness or confusion (J.L. Price, J.C. Morris, Annals of Neurology, 45:358-68, March 1999). John C. Morris, the Harvey A. and Dorismae Hacker Friedman professor of neurology, and Joseph L. Price, professor of anatomy and neurobiology, both of the Washington University School of Medicine in St. Louis, monitored cognitive ability in 62 patients, then examined their brains after death. All the participants had tangles, but plaques were more clearly linked to dementia. Seven of the 39 people who had shown no signs of dementia but nevertheless had some plaques and excess tangles caught the researchers' attention. "We think they had preclinical Alzheimer's disease," says Morris. The plaques possibly stimulated tangle formation, Price adds. Dissecting the beginnings of Alzheimer's could have practical implications. "Effective therapy may need to occur before clinical signs are apparent. The lesions, if arrested in the preclinical stage, may not always result in symptomatic disease," concludes Morris.
CONNECTING CHLAMYDIA TO HEART DISEASE If there aren't already enough reasons to practice "safe sex," here's another: Researchers at the Ontario Cancer Institute in Toronto have established a causal link between chlamydia and heart disease (K. Bachmaier et al., Science, 283:1335-9, Feb. 26, 1999). In a mouse model study, the researchers found that the bacterium uses antigenic mimicry to evade the immune system. One piece of a protein on chlamydia's surface closely resembles another piece of protein in the heart muscle myosin, setting the stage for a molecular case of mistaken identity. "In the process of fighting the bacterial infection the immune system attacks the protein myosin, mistaking it for the chlamydia bacteria," explains Kurt Bachmaier. That mistake ultimately leads to inflammatory heart disease. The study suggests that some cases of heart disease could be prevented by antibiotic treatment and immunization, Bachmaier notes. But he cautions that this mechanism only occurs in certain mouse strains--meaning it may not be universal for humans. "The single most important factor to confer susceptibility to this kind of disease in the mouse is the molecule called major histocompatability complex," he explains. Human populations contain a wide variability in these molecules, which may explain why everyone infected with chlamydia doesn't get heart disease. While Bachmaier and colleagues are now investigating human blood samples for antibodies reactive to chlamydia, three other large trials, involving more than 8,000 heart disease patients, are under way to determine if antibiotics effective against chlamydia will reduce the risk of heart attacks.
|Kiochi Shimizu, University of Michigan|
|Melanoma metastases appear as black nodules in the lungs of mice in the University of Michigan study (left). Lungs from mice treated with the dendritic cell vaccine and interleukin-2 show no evidence of residual disease (right).|
IRON-HEAVY RICE Rice seeds genetically engineered in Japan to contain as much as three times their normal iron levels may one day help reduce widespread anemia among people with cereal-based diets. Researchers from three institutes have collaborated to transfer the entire coding sequence of the soybean ferritin gene into the endosperm of rice seeds (F. Goto et al., Nature Biotechnology, 17:282-6, March 1999). Ferritin, a protein highly efficient at storing iron, was introduced with the help of a gene promoter that switches on expression in the rice seed. "The mechanism to store much of the iron in the ferritin is still unclear, and ... the amount of iron stored in the ferritin is variable among the cultures," cautions coauthor Toshihiro Yoshihara , a plant scientist at the Central Research Institute Electric Power Industry (CRIEPI) in Chiba, Japan. He says that the explanation for this variability and its relation to rice culture conditions still must be explored. Understanding the mechanism by which ferritin stores iron might lead to increased iron storage in the transgenic rice, he adds. Yoshihara's group also intends to study "the actual effect of iron in ferritin on human anemia." Although the iron-fortified rice itself has not been patented, CRIEPI is applying in Japan to patent crops produced with the technology.