RECON syndrome is a genome instability disorder caused by mutations in the DNA helicase RECQL1.

Despite being the first homolog of the bacterial RecQ helicase to be identified in humans, the function of RECQL1 remains poorly characterized. Furthermore, unlike other members of the human RECQ family of helicases, mutations in RECQL1 have not been associated with a genetic disease. Here, we identify 2 families with a genome instability disorder that we have named RECON (RECql ONe) syndrome, caused by biallelic mutations in the RECQL gene.

The Promotion of Genomic Instability in Human Fibroblasts by Adenovirus 12 Early Region 1B 55K Protein in the Absence of Viral Infection.

The adenovirus 12 early region 1B55K (Ad12E1B55K) protein has long been known to cause non-random damage to chromosomes 1 and 17 in human cells. These sites, referred to as Ad12 modification sites, have marked similarities to classic fragile sites. In the present report we have investigated the effects of Ad12E1B55K on the cellular DNA damage response and on DNA replication, considering our increased understanding of the pathways involved.

Metabolic mechanisms of indoxacarb resistance in field populations of Choristoneura rosaceana (Harris) (Lepidoptera: Tortricidae).

Synergism and metabolic studies were conducted to identify the resistance mechanism against indoxacarb in two Choristoneura rosaceana (Harris) field populations compared to a susceptible population. The synergism study was carried out using diet incorporation bioassay for indoxacarb and the three synergists PBO, DEM, and DEF. The metabolic study consists of indoxacarb in vitro reaction with fifth instar larvae 12,000 g midgut supernatant or with pre-inhibited (in vivo by the esterases inhibitor DEF) fifth instar larvae 12,000 g midgut supernatant at different incubation times.

Productive herpesvirus lytic replication in primary effusion lymphoma cells requires S-phase entry.

Gammaherpesviruses establish lifelong latent infection in B lymphocytes and are the causative agent of several B-cell malignancies and lymphoproliferative disorders. While a quiescent latent infection allows these pathogens to evade immune detection, initiation of an alternative lifecycle stage, known as lytic replication, is an essential step in the production and dissemination of infectious progeny. Although cessation of cellular proliferation is an eventual consequence of lytic induction, exactly how gammaherpesviruses manipulate the cell cycle prior to amplification of viral DNA remains under debate.