In work appearing this week in PNAS, Stanford University's Jerrod Schwartz and Stephen Quake show that they can use single molecule measurements to find the "speed limit" of DNA polymerase. By observing both the burst synthesis rate and pausing events, they found that for E. coli DNA Polymerase I (KF), the strand displacement burst synthesis rate was one order of magnitude faster than the reported bulk strand displacement rate, "a discrepancy that can be accounted for by sequence specific pausing," they say. Their observations also showed that the burst synthesis rate can vary up to 50-fold from molecule to molecule.
A team of scientists led by those at the Albert Einstein College of Medicine in New York has found that a certain group of Ashkenazi Jewish centenarians share the trait of having longer telomeres and genetic variations in telomerase genes. Telomere shortening has been associated with diseases of aging. In this paper, sequence analysis of two major genes associated with telomerase activity, hTERT and hTERC, showed "overrepresentation of synonymous and intronic mutations among centenarians relative to controls," they say. "Moreover, we identified a common hTERT haplotype that is associated with both exceptional longevity and longer telomere length." The findings, says a story at BBC, suggest that "telomere length and variants of telomerase genes combine to help people live very long lives, perhaps by protecting them from the diseases of old age," they say.
University of California, San Francisco, scientists studied how prion protein conformation affects its activity in a host cell. Led by Stanley Prusiner, they made an array of recombinant PrP amyloids with different stabilities and saw that when put into mice the most stable amyloids produced the most stable prion strains with the longest incubation times, while more labile amyloids produced less stable strains and shorter incubation times. "The direct relationship between stability and incubation time of prion strains suggests that labile prions are more fit, in that they accumulate more rapidly and thus kill the host faster," they say.
Finally, work from David Baltimore at Cal Tech and Pin Wang at the University of Southern California used a lentivector-based vaccine to induce a type of HIV-1 immunity in dendritic cells. The system encodes the HIV Gag protein, and the cellular specificity comes about "through pseudotyping the vector with an engineered Sindbis virus glycoprotein capable of selectively binding to the DC-SIGN protein," they say. Their results show that one immunization by this vector can induce an HIV Gag-specific immune response in mice.