Predation of artificial Sage Grouse nests in treated and untreated sagebrush

We measured predation on 120 artificial Sage Grouse ( Centrarcus urophasianus ) nests in montane sagebrush grassland in northern Utah. We examined nests in areas that had been chained and seeded 25 years previously (treated areas) and in areas that were untreated. Predation rates of artificial nests were higher in areas of untreated sagebrush, even though these areas had greater sagebrush cover, taller shrubs, and greater horizontal plant cover. These results differ from those previously hypothesized for treated sagebrush habitat and may reflect a greater abundance of other potential prey species, especially lagomorphs, in untreated areas that attracted greater densities of predators. In addition, over 80% of nests were depredated by mammals, which hunt using olfaction and are less likely than avian predators to be affected by nest cover. We conclude that, after treated sagebrush has recovered to some degree, predation rates of Sage Grouse nests may be lower in treated sagebrush. Consequently, factors other than nest predation (e.g., winter food, thermal cover, insects, perennial forb abundance) may be more important reasons for preserving mature sagebrush stands for Sage Grouse.     

Reproductive ecology of bison on Antelope Island, Utah

Autumn musters of bison ( Bison bison ) on Antelope Island State Park, Utah, conducted annually since 1987, provided data on temporal and age-specific reproductive patterns and a basis to evaluate the efficacy of management measures implemented to elevate reproductive performance in the herd. Pregnancy rates were variable and low ( x = 46.2%) in comparison to other free-ranging, noncommercial bison herds in North America. Cows in the 3- and > 6-yr range age classes exhibited lower-than-expected pregnancy rates ( P r = 0.64, P = 0.047) linear decline of 2.5% per annum. Variance in distribution of fetal ages observed in 6 yr indicates substantial temporal fluctuation. Long-term reproductive performance of cohorts born prior to implementation of management measures did not differ from that of cohorts born subsequent to these changes.     

Morphological transformation in vivo of human uterine cervix with papillomavirus from condylomata acuminata

Carcinoma of the human uterine cervix has been associated with several infectious agents including papillomavirus. Papillomavirus group-specific antigen (GSA) and viral particles have been demonstrated in human condylomata acuminata (CA) and flat warts of the uterine cervix. Cell alterations consisting of nuclear enlargement, hyperchromasia, irregularity, binucleation and cytoplasmic clearing (koilocytosis) are often interpreted as mild to moderate dysplasia. Present evidence that human papillomavirus (HPV) is responsible for the development of these lesions relies on the association of GSA and virus particles in the affected tissue, fulfilling the first two of Koch's postulates. Direct proof of an aetiological relationship, however, requires induction of the CA change in normal, human uterine cervix after exposure to papillomavirus. Infecting human subjects with HPV is ethically unacceptable and no satisfactory alternative systems have been defined. Also, human cell cultures do not support growth or transformation by HPV. Here we report the first demonstration of the morphological transformation of human tissues with a human papillomavirus under controlled, experimental conditions. 'Transformation' is used here in its literal sense to refer to a heritable morphological alteration in the appearance of the cells. The use of this term does not indicate that the changes described are neoplastic, but they are identical to the dysplastic changes found in biopsies of uterine cervical CA. Our results demonstrate the direct involvement of CA virus in dysplastic change of human cervical tissue and indicate that the experimental system described may be useful in elucidating the contribution of human papillomaviruses to the pathogenesis of human cervical cancer.     

Spatially scaled response of a Lazuli Bunting population to fire

We examined the response of Lazuli Bunting ( Passerina amoena ) to fire in Gambel oak ( Quercus gambelii ) woodland at Camp Williams, Utah, during 1993–1998. Overall, Lazuli Bunting abundance on the study area increased significantly during the 2 years after a stand-replacing wildfire, which covered 800 ha of Gambel oak woodland. This increase suggested that Lazuli Buntings respond positively to fire. However, a comparison of pre- and postfire abundance of Lazuli Bunting for 2 groups of monitoring plots with different fire histories showed that abundance was significantly greater during the post-fire period for both burned and unburned plots. When we examined our data at a spatial scale appropriate to Lazuli Bunting, we found that post-fire increases observed on unburned plots were limited to plots in close proximity to the burned area. A comparison of pre- and post-fire abundance of Lazuli Bunting for 3 groups of monitoring plots located at various distances from the burned area revealed that post-fire abundance was similar only for plots within the fire boundary and for those ≤1000 m from the fire boundary; plots located >1000 m from the fire boundary had fewer individuals per plot post-fire. However, prefire Lazuli Bunting abundance was similar among all 3 categories. This differential, spatially scaled response of Lazuli Bunting to fire at the landscape level may support a hierarchical view of habitat selection.     

A presenilin-1-dependent gamma-secretase-like protease mediates release of Notch intracellular domain

Signalling through the receptor protein Notch, which is involved in crucial cell-fate decisions during development, requires ligand-induced cleavage of Notch. This cleavage occurs within the predicted transmembrane domain, releasing the Notch intracellular domain (NICD), and is reminiscent of gamma-secretase-mediated cleavage of beta-amyloid precursor protein (APP), a critical event in the pathogenesis of Alzheimer's disease. A deficiency in presenilin-1 (PS1) inhibits processing of APP by gamma-secretase in mammalian cells, and genetic interactions between Notch and PS1 homologues in Caenorhabditis elegans indicate that the presenilins may modulate the Notch signalling pathway. Here we report that, in mammalian cells, PS1 deficiency also reduces the proteolytic release of NICD from a truncated Notch construct, thus identifying the specific biochemical step of the Notch signalling pathway that is affected by PS1. Moreover, several gamma-secretase inhibitors block this same step in Notch processing, indicating that related protease activities are responsible for cleavage within the predicted transmembrane domains of Notch and APP. Thus the targeting of gamma-secretase for the treatment of Alzheimer's disease may risk toxicity caused by reduced Notch signalling.     

CD4+ T cells are required for secondary expansion and memory in CD8+ T lymphocytes

A long-standing paradox in cellular immunology concerns the conditional requirement for CD4+ T-helper (T(H)) cells in the priming of cytotoxic CD8+ T lymphocyte (CTL) responses in vivo. Whereas CTL responses against certain viruses can be primed in the absence of CD4+ T cells, others, such as those mediated through 'cross-priming' by host antigen-presenting cells, are dependent on T(H) cells. A clearer understanding of the contribution of T(H) cells to CTL development has been hampered by the fact that most T(H)-independent responses have been demonstrated ex vivo as primary cytotoxic effectors, whereas T(H)-dependent responses generally require secondary in vitro re-stimulation for their detection. Here, we have monitored the primary and secondary responses of T(H)-dependent and T(H)-independent CTLs and find in both cases that CD4+ T cells are dispensable for primary expansion of CD8+ T cells and their differentiation into cytotoxic effectors. However, secondary CTL expansion (that is, a secondary response upon re-encounter with antigen) is wholly dependent on the presence of T(H) cells during, but not after, priming. Our results demonstrate that T-cell help is 'programmed' into CD8+ T cells during priming, conferring on these cells a hallmark of immune response memory: the capacity for functional expansion on re-encounter with antigen.