Nest of Formica propinqua (Hymenoptera: Formicidae)

The nest of the ant Formica propinqua W. M. Wheeler is reported from Washoe Co., Nevada.     

Habitat use of leatherside chub ( Gila copei ) in the presence of predatory brown trout ( Salmo trutta )

The objectives of this study were to (1) examine distribution and habitat use of leatherside chub ( Gila copei ) in a creek with high densities of predatory brown trout ( Salmo trutta ), and (2) compare study results with published accounts of leatherside chub habitat use in streams with few or no brown trout. A 14-km section of Diamond Fork Creek, Utah, was point-shocked to determine macrohabitat (main channel and lateral habitat) and microhabitat (current, depth, substrate, and cover) use of leatherside chug. At the macrohabitat level, leatherside chub were most common in lower reaches of Diamond Fork Creek where the channel was braided and lateral habitats (cutoff pools and backwaters) were abundant. Only a single leatherside chub was found in the main channel of Diamond Fork. Investigations in other systems lacking brown trout indicated that leatherside chub occupy main channel habitats. At the microhabitat level, we found significant positive associations between presence of leatherside chub and both habitat depth and silt. In addition, we found a significant negative association between presence of leatherside chub and number of brown trout. Our results suggest predation by brown trout may limit leatherside chub to lateral habitats that could provide refugia against predation. The introduction of brown trout to systems with little lateral habitat could have serious effects on persistence of resident leatherside chub populations.     

Survivorship and cause-specific mortality in five populations of mule deer

We used retrospective analyses to investigate cause-specific mortality and survivorship among 5 populations of mule deer ( N = 168 telemetered animals) wintering in the western Great Basin during 1986-1994. These populations existed under similar environmental conditions, but survivorship functions differed among them. Monthly survival ranged from 0.964 to 0.990, and annual survival ranged from 0.643 to 0.884. The proportion of deaths attributed to predation and malnutrition or anthropogenic causes did not differ among the 5 populations. Predation was the leading cause of mortality; mountain lions were responsible for approximately 90% of the deer killed by predators. No difference existed among these populations in the proportion of telemetered deer that were killed by mountain lions, but proportionally more females than males were killed by these large fields. Predation by mountain lions is the primary source of mortality and a widespread phenomenon among the populations of mule deer we investigated.     

Occurrence of ticks on mule deer in central Utah

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Identification of a bacterial inhibitor against g-type lysozyme

Lysozymes are antibacterial effectors of the innate immune system in animals that hydrolyze peptidoglycan. Bacteria have evolved protective mechanisms that contribute to lysozyme tolerance such as the production of lysozyme inhibitors, but only inhibitors of chicken (c-) and invertebrate (i-) type lysozyme have been identified. We here report the discovery of a novel Escherichia coli inhibitor specific for goose (g-) type lysozymes, which we designate PliG (periplasmic lysozyme inhibitor of g-type lysozyme). Although it does not inhibit c- or i-type lysozymes, PliG shares a structural sequence motif with the previously described PliI and MliC/PliC lysozyme inhibitor families, suggesting a common ancestry and mode of action. Deletion of pliG increased the sensitivity of E. coli to g-type lysozyme. The existence of inhibitors against all major types of animal lysozyme and their contribution to lysozyme tolerance suggest that lysozyme inhibitors may play a role in bacterial interactions with animal hosts.     

A single EFEMP1 mutation associated with both Malattia Leventinese and Doyne honeycomb retinal dystrophy.

Malattia Leventinese (ML) and Doyne honeycomb retinal dystrophy (DHRD) refer to two autosomal dominant diseases characterized by yellow-white deposits known as drusen that accumulate beneath the retinal pigment epithelium (RPE). Both loci were mapped to chromosome 2p16-21 (refs 5,6) and this genetic interval has been subsequently narrowed. The importance of these diseases is due in large part to their close phenotypic similarity to age-related macular degeneration (AMD), a disorder with a strong genetic component that accounts for approximately 50% of registered blindness in the Western world. Just as in ML and DHRD, the early hallmark of AMD is the presence of drusen. Here we use a combination of positional and candidate gene methods to identify a single non-conservative mutation (Arg345Trp) in the gene EFEMP1 (for EGF-containing fibrillin-like extracellular matrix protein 1) in all families studied. This change was not present in 477 control individuals or in 494 patients with age-related macular degeneration. Identification of this mutation may aid in the development of an animal model for drusen, as well as in the identification of other genes involved in human macular degeneration.     

Epidermal growth factor receptor function is necessary for normal craniofacial development and palate closure.

Craniofacial malformations are among the most frequent congenital birth defects in humans; cleft palate, that is inadequate fusion of the palatal shelves, occurs with an annual incidence of 1 in 700 to 1 in 1,000 live births among individuals of European descent. The secondary palate arises as bilateral outgrowths from the maxillary processes, and its formation depends on the coordinated development of craniofacial structures including the Meckel's cartilage and the mandible. Cleft lip and palate syndromes in humans are associated with polymorphisms in the gene (TGFA) encoding transforming growth factor-alpha (TGF-alpha), an epidermal growth factor receptor (EGFR) ligand made by most epithelia. Here we have characterized craniofacial development in Egfr-deficient (Egfr-/-) mice. Newborn Egfr-/- mice have facial mediolateral defects including narrow, elongated snouts, underdeveloped lower jaw and a high incidence of cleft palate. Palatal shelf explants from Egfr-/- mice fused, but frequently had residual epithelium in the midline. In addition, morphogenesis of Meckel's cartilage was deficient in cultured mandibular processes from Egfr-/- embryos. The secretion of matrix metalloproteinases (MMPs) was diminished in Egfr-/- explants, consistent with the ability of EGF to increase MMP secretion and with the decreased MMP expression caused by inhibition of Egfr signalling in wild-type explants. Accordingly, inactivation of MMPs in wild-type explants phenocopied the defective morphology of Meckel's cartilage seen in Egfr-/- explants. Our results indicate that EGFR signalling is necessary for normal craniofacial development and that its role is mediated in part by its downstream targets, the MMPs, and may explain the genetic correlation of human cleft palate with polymorphisms in TGFA.