EU Borders and Their Controls: Preventing unwanted movement of people in Europe? CEPS Essay No. 6, 14 November 2013

his Essay attempts to take a step back from the tragic event in the first week of October 2013, when a boat capsized off the Italian island of Lampedusa and some 300 persons drowned seeking safe harbour. It sets out to examine the issue of EU border controls from the perspectives of the technologies, new and old, building on a variety of scholarly disciplines to understand what is happening to border controls on the movement of persons in the EU and why the results are so deadly. The Essay opens with an overview of what actually happens at the EU’s external borders. It then moves on to assess the old and new set of border control technologies that are deployed at the EU external borders, and how new technologies such as those based on automated controls and biometrics, are transforming the classical principles of European border controls. It then covers the reasons why people are refused admission at the EU’s external borders and the extent to which new border and surveillance technologies would assist in the effective controls in light of EU border law. Conclusions are finally offered on the articulation between the facts of EU border controls on persons and the claims and proposals for new technologies that are emerging from the EU institutions.

Polo-like kinase 4 controls centriole duplication but does not directly regulate cytokinesis

Centrioles organize the centrosome, and accurate control of their number is critical for the maintenance of genomic integrity. Centrioles duplicate once per cell cycle, and duplication is coordinated by Polo-like kinase 4 (Plk4). We previously demonstrated that Plk4 accumulation is autoregulated by its own kinase activity. However, loss of heterozygosity of Plk4 in mouse embryonic fibroblasts has been proposed to cause cytokinesis failure as a primary event, leading to centrosome amplification and gross chromosomal abnormalities. Using targeted gene disruption, we show that human epithelial cells with one inactivated Plk4 allele undergo neither cytokinesis failure nor increase in centrosome amplification. Plk4 is shown to localize exclusively at the centrosome, with none in the spindle midbody. Substantial depletion of Plk4 by small interfering RNA leads to loss of centrioles and subsequent spindle defects that lead to a modest increase in the rate of cytokinesis failure. Therefore, Plk4 is a centriole-localized kinase that does not directly regulate cytokinesis.