NLO thermal dilepton rate at non-zero momentum

The vector channel spectral function and the dilepton production rate from a QCD plasma at a temperature above a few hundred MeV are evaluated up to next-to-leading order (NLO) including their dependence on a non-zero momentum with respect to the heat bath. The invariant mass of the virtual photon is taken to be in the range K2 ~ (πT)2 ~ (1GeV)2, generalizing previous NLO results valid for K2 ≫ (πT)2. In the opposite regime 0 < K2 ≪ (πT)2 the loop expansion breaks down, but agrees nevertheless in order of magnitude with a previous result obtained through resummations. Ways to test the vector spectral function through comparisons with imaginary-time correlators measured on the lattice are discussed.

The Drosophila chk2 gene loki is essential for embryonic DNA double-strand-break checkpoints induced in S phase or G2

Cell cycle checkpoints are signal transduction pathways that control the order and timing of cell cycle transitions, ensuring that critical events are completed before the occurrence of the next cell cycle transition. The Chk2 family of kinases is known to play a central role in mediating the cellular responses to DNA damage or DNA replication blocks in various organisms. Here we show through a phylogenetic study that the Drosophila melanogaster serine/threonine kinase Loki is the homolog of the yeast Mek1p, Rad53p, Dun1p, and Cds1 proteins as well as the human Chk2. Functional analyses allowed us to conclude that, in flies, chk2 is involved in monitoring double-strand breaks (DSBs) caused by irradiation during S and G2 phases. In this process it plays an essential role in inducing a cell cycle arrest in embryonic cells. Our results also show that, in contrast to C. elegans chk2, Drosophila chk2 is not essential for normal meiosis and recombination, and it also appears to be dispensable for the MMS-induced DNA damage checkpoint and the HU-induced DNA replication checkpoint during larval development. In addition, Drosophila chk2 does not act at the same cell cycle phases as its yeast homologs, but seems rather to be involved in a pathway similar to the mammalian one, which involves signaling through the ATM/Chk2 pathway in response to genotoxic insults. As mutations in human chk2 were linked to several cancers, these similarities point to the usefulness of the Drosophila model system.