In this week's issue of Science, Rockefeller University researchers Richard Pomerantz and Mike O'Donnell report that Escherichia coli replication forks that have stalled following head-on collisions with RNA polymerase remain stable and can restart once the polymerase is ousted by a transcription-repair coupling factor Mfd. "These findings demonstrate the intrinsic stability of the replication apparatus and a previously unknown role for the transcription-coupled repair pathway in promoting replication past a [RNA polymerase] block," they write.
An international research team, including investigators from Monsanto, found a pathway involved in seed dessication tolerance in bryophytes such as moss and angiosperms. In both types of plants, they report, seed dessication tolerance seems to rely on the hormone abscisic acid and a transcriptional regulator called abscisic acid insensitive 3 or ABI3, with abscisic acid treatment inducing at least 22 genes.
MIT researcher Tyler Jacks and his co-workers used gene deletion studies to identify a role for p53 in gastrointestinal damage in mice after exposure to ionizing radiation. While mice lacking p53 in their GI epithelial cells were sensitive to this damage, those over-expressing p53 were protected from the GI syndrome. Knocking out two pro-apoptotic genes, on the other hand, had no effect. "These results suggest that the GI syndrome is caused by the death of GI epithelial cells and that these epithelial cells die by a mechanism that is regulated by p53 but independent of apoptosis," they write.
Meanwhile, in the advance, online edition of the journal, researchers from the US and China demonstrate the infectivitiy of misfolded prion protein by expressing a recombinant mouse prion protein in E. coli and using it to infect wild type mice. Consistent with the prion hypothesis, they show that this recombinant protein can cause prion disease in the mice.