High seroprevalence against lawsonia intracellularis among adult horses in Belgium

peer reviewedLawsonia intracellularis (LI) is an obligate intracellular gram-negative rod causing equine proliferative enteropathy (EPE). Occasional cases of EPE have been reported in foals living in Belgium, but the seroprevalence of equine LI in this country is unknown. The target population included clinically healthy adult horses, whose blood samples were collected and analysed for specific IgG antibodies against LI using a blocking enzyme-linked immunosorbent assay (bELISA) test. Results were expressed as Percentage of Inhibition (PI). Samples that had a PI 30% were considered positive. A total of 356 blood samples were analysed with 352 horses (98.8%) testing positive, 2 horses (0. 6%) testing negative and 2 horses (0.6%) showing inconclusive results. The large percentage of seropositive samples obtained in this study confirms a widespread exposure of Belgian horses to LI

TRF2-Mediated Control of Telomere DNA Topology as a Mechanism for Chromosome-End Protection.

International audienceThe shelterin proteins protect telomeres against activation of the DNA damage checkpoints and recombinational repair. We show here that a dimer of the shelterin subunit TRF2 wraps ∼ 90 bp of DNA through several lysine and arginine residues localized around its homodimerization domain. The expression of a wrapping-deficient TRF2 mutant, named Top-less, alters telomeric DNA topology, decreases the number of terminal loops (t-loops), and triggers the ATM checkpoint, while still protecting telomeres against non-homologous end joining (NHEJ). In Top-less cells, the protection against NHEJ is alleviated if the expression of the TRF2-interacting protein RAP1 is reduced. We conclude that a distinctive topological state of telomeric DNA, controlled by the TRF2-dependent DNA wrapping and linked to t-loop formation, inhibits both ATM activation and NHEJ. The presence of RAP1 at telomeres appears as a backup mechanism to prevent NHEJ when topology-mediated telomere protection is impaired