Birth,Death, and Diversification of Mobile Promoters in Prokaryotes

A previous study of prokaryotic genomes identified large reservoirs of putative mobile promoters (PMPs), that is, homologous promoter sequences associated with nonhomologous coding sequences. Here we extend this data set to identify the full complement of mobile promoters in sequenced prokaryotic genomes. The expanded search identifies nearly 40,000 PMP sequences, 90% of which occur in noncoding regions of the genome. To gain further insight from this data set, we develop a birth–death–diversification model for mobile genetic elements subject to sequence diversification; applying the model to PMPs we are able to quantify the relative importance of duplication, loss, horizontal gene transfer (HGT), and diversification to the maintenance of the PMP reservoir. The model predicts low rates of HGT relative to the duplication and loss of PMP copies, rapid dynamics of PMP families, and a pool of PMPs that exist as a single copy in a genome at any given time, despite their mobility. We report evidence of these “singletons” at high frequencies in prokaryotic genomes. We also demonstrate that including selection, either for or against PMPs, was not necessary to describe the observed data.     

Damage and repair in mammalian cells after exposure to non-ionizing radiations III. Ultraviolet and visible light irradiation of cells of placental mammals,including humans,and determinations of photorepairable damage in vitro

Cultured cells of placental mammals (including human skin fibroblasts) as well as fresh cornea tissue from oxen have been UV (254 nm)-irradiated and either kept dark or exposed to photoreactivating light (wavelengths >375 nm) only prior to extraction of their DNA. The latter was added to an in vitro photorepair system consisting of UV-irradiated DNA from Haemophilus influenzae and yeast-photoreactivating enzyme, illuminated with broad-spectrum white fluorescent light. The extent of competitive inhibition of the in vitro photorepair of Haemophilus-DNA, resulting from the addition of mammalian DNA, has been taken as a measure of mammalian DNA lesions capable of reacting with photoreactivating enzyme. In most cases the amount of these DNA lesions was reduced if the UV-irradiated mammalian cells had been light-exposed prior to DNA extraction, indicating photoenzymatic repair of up to 90% of the lesions. DNA damage by the photoreactivating light itself was observed at varying degrees in human cells, where this effect presumably masks some of the photorepair.