The bornavirus-derived human protein EBLN1 promotes efficient cell cycle transit, microtubule organisation and genome stability.

It was recently discovered that vertebrate genomes contain multiple endogenised nucleotide sequences derived from the non-retroviral RNA bornavirus. Strikingly, some of these elements have been evolutionary maintained as open reading frames in host genomes for over 40 million years, suggesting that some endogenised bornavirus-derived elements (EBL) might encode functional proteins. EBLN1 is one such element established through endogenisation of the bornavirus N gene (BDV N). Here, we functionally characterise human EBLN1 as a novel regulator of genome stability. Cells depleted of human EBLN1 accumulate DNA damage both under non-stressed conditions and following exogenously induced DNA damage. EBLN1-depleted cells also exhibit cell cycle abnormalities and defects in microtubule organisation as well as premature centrosome splitting, which we attribute in part, to improper localisation of the nuclear envelope protein TPR. Our data therefore reveal that human EBLN1 possesses important cellular functions within human cells, and suggest that other EBLs present within vertebrate genomes may also possess important cellular functions.

[Cellular and molecular mechanisms of the effect of polymetallic dust on the respiratory organs]. / Kletochno-molekuliarnye mekhanizmy deistviia polimetallicheskoi pyli na organy dykhaniia.

During the experiment on 158 white rats the mechanism of impact of lead and zinc concentrated dust on the respiratory system was studied by means of its single intratracheal administration into the lungs. The character of metabolic processes in phagocytes and the state of the most important systems of cellular energy supply were determined. The established character enabled one to detect the basic cellular impairments caused by dust effect. The major chains of dust toxic effect at the cellular and molecular level were demonstrated.