Nearctic \u3ci\u3eAcleris\u3c/i\u3e: Resurrection of \u3ci\u3eA. Stadiana\u3c/i\u3e and a Revised Identity for \u3ci\u3eA. Semiannula\u3c/i\u3e (Lepidoptera: Tortricidae)

Type study showed that Acleris stadiana (Barnes & Busck), currently considered a junior synonym of A. semiannula (Robinson), is in fact a distinct taxon. Although superficially similar, these taxa differ markedly in genital structure. In males of A. semiannula, the aedeagus is short, broad, and virtually straight, whereas in those of A. stadiana, it is long, thin, and sharply bent. What was known in literature as A. semiannula proved to be A. stadi­ana. We redefine both A. semiannula and the resurrected A. stadiana

\u3ci\u3eAmphiphala\u3c/i\u3e, a New Genus and Its Three New Species from Eastern North America (Lepidoptera: Tortricidae: Cochylina)

Amphiphala Roberts and Sabourin, new genus (Lepidoptera: Tortricidae), is proposed for three new species: A. liatriana Roberts and Sabourin, new species; A. landryana Brown, new species; and A. carolana Sabourin, new species. The genus is recorded from the eastern part of North America from Ontario, Canada south to South Carolina, and west to Manitoba and Mississippi. Owing to its superficial similarity to the banded sunflower moth, Cochylichroa hospes (Walsingham, 1884), Amphiphala remained hidden in North American Lepidoptera collections. Amphiphala liatriana has been reared from northern blazing star, Liatris scariosa (L.) Willd. (Asteraceae), in Maine

Conserved host response to highly pathogenic avian influenza virus infection in human cell culture, mouse and macaque model systems

<p>Abstract</p> <p>Background</p> <p>Understanding host response to influenza virus infection will facilitate development of better diagnoses and therapeutic interventions. Several different experimental models have been used as a proxy for human infection, including cell cultures derived from human cells, mice, and non-human primates. Each of these systems has been studied extensively in isolation, but little effort has been directed toward systematically characterizing the conservation of host response on a global level beyond known immune signaling cascades.</p> <p>Results</p> <p>In the present study, we employed a multivariate modeling approach to characterize and compare the transcriptional regulatory networks between these three model systems after infection with a highly pathogenic avian influenza virus of the H5N1 subtype. Using this approach we identified functions and pathways that display similar behavior and/or regulation including the well-studied impact on the interferon response and the inflammasome. Our results also suggest a primary response role for airway epithelial cells in initiating hypercytokinemia, which is thought to contribute to the pathogenesis of H5N1 viruses. We further demonstrate that we can use a transcriptional regulatory model from the human cell culture data to make highly accurate predictions about the behavior of important components of the innate immune system in tissues from whole organisms.</p> <p>Conclusions</p> <p>This is the first demonstration of a global regulatory network modeling conserved host response between <it>in vitro </it>and <it>in vivo </it>models.</p

A Novel Checkpoint and RPA Inhibitory Pathway Regulated by Rif1

Cells accumulate single-stranded DNA (ssDNA) when telomere capping, DNA replication, or DNA repair is impeded. This accumulation leads to cell cycle arrest through activating the DNA–damage checkpoints involved in cancer protection. Hence, ssDNA accumulation could be an anti-cancer mechanism. However, ssDNA has to accumulate above a certain threshold to activate checkpoints. What determines this checkpoint-activation threshold is an important, yet unanswered question. Here we identify Rif1 (Rap1-Interacting Factor 1) as a threshold-setter. Following telomere uncapping, we show that budding yeast Rif1 has unprecedented effects for a protein, inhibiting the recruitment of checkpoint proteins and RPA (Replication Protein A) to damaged chromosome regions, without significantly affecting the accumulation of ssDNA at those regions. Using chromatin immuno-precipitation, we provide evidence that Rif1 acts as a molecular “band-aid” for ssDNA lesions, associating with DNA damage independently of Rap1. In consequence, small or incipient lesions are protected from RPA and checkpoint proteins. When longer stretches of ssDNA are generated, they extend beyond the junction-proximal Rif1-protected regions. In consequence, the damage is detected and checkpoint signals are fired, resulting in cell cycle arrest. However, increased Rif1 expression raises the checkpoint-activation threshold to the point it simulates a checkpoint knockout and can also terminate a checkpoint arrest, despite persistent telomere deficiency. Our work has important implications for understanding the checkpoint and RPA–dependent DNA–damage responses in eukaryotic cells

p38-γ–dependent gene silencing restricts entry into the myogenic differentiation program

The regenerative capacity of muscle is regulated by p38-γ, which phosphorylates MyoD and leads to formation of a complex that represses myogenin transcription

Nearctic \u3ci\u3eAcleris\u3c/i\u3e: Resurrection of \u3ci\u3eA. Stadiana\u3c/i\u3e and a Revised Identity for \u3ci\u3eA. Semiannula\u3c/i\u3e (Lepidoptera: Tortricidae)

Type study showed that Acleris stadiana (Barnes & Busck), currently considered a junior synonym of A. semiannula (Robinson), is in fact a distinct taxon. Although superficially similar, these taxa differ markedly in genital structure. In males of A. semiannula, the aedeagus is short, broad, and virtually straight, whereas in those of A. stadiana, it is long, thin, and sharply bent. What was known in literature as A. semiannula proved to be A. stadi­ana. We redefine both A. semiannula and the resurrected A. stadiana