Individual return patterns of spawning flannelmouth sucker (Catostomus latipinnis) to a desert river tributary.

Tributaries provide temporal and spatial habitat heterogeneity in river networks that can be critical for parts of the life history of a species. Tributary fidelity can benefit individual fish undergoing spawning migrations by reducing time and energy spent exploring new areas and leveraging previous experience, but anthropogenic activities that fragment or degrade these systems can eliminate those benefits. We used multistate models based on passive integrated transponder (PIT) detection data from 2013 to 2023 to estimate the proportion of flannelmouth suckers (Catostomus latipinnis) migrating to a tributary, McElmo Creek, from the mainstem San Juan River for spawning.

Migration timing and tributary use of spawning flannelmouth sucker (Catostomus latipinnis).

Spawning phenology and associated migrations of fishes are often regulated by factors such as temperature and stream discharge, but flow regulation of mainstem rivers coupled with climate change might disrupt these cues and affect fitness. Flannelmouth sucker (Catostomus latipinnis) persisting in heavily modified river networks are known to spawn in tributaries that might provide better spawning habitat than neighboring mainstem rivers subject to habitat degradation (e.g.

Splicing factor deficits render hematopoietic stem and progenitor cells sensitive to STAT3 inhibition.

Hematopoietic stem and progenitor cells (HSPCs) sustain lifelong hematopoiesis. Mutations of pre-mRNA splicing machinery, especially splicing factor 3b, subunit 1 (SF3B1), are early lesions found in malignancies arising from HSPC dysfunction. However, why splicing factor deficits contribute to HSPC defects remains incompletely understood.

Exploring metapopulation-scale suppression alternatives for a global invader in a river network experiencing climate change.

Invasive species can dramatically alter ecosystems, but eradication is difficult, and suppression is expensive once they are established. Uncertainties in the potential for expansion and impacts by an invader can lead to delayed and inadequate suppression, allowing for establishment. Metapopulation viability models can aid in planning strategies to improve responses to invaders and lessen invasive species' impacts, which may be particularly important under climate change.

Intrahepatic microbes govern liver immunity by programming NKT cells.

The gut microbiome shapes local and systemic immunity. The liver is presumed to be a protected sterile site. As such, a hepatic microbiome has not been examined.

Definitive hematopoietic stem cells minimally contribute to embryonic hematopoiesis.

Hematopoietic stem cells (HSCs) are rare cells that arise in the embryo and sustain adult hematopoiesis. Although the functional potential of nascent HSCs is detectable by transplantation, their native contribution during development is unknown, in part due to the overlapping genesis and marker gene expression with other embryonic blood progenitors. Using single-cell transcriptomics, we define gene signatures that distinguish nascent HSCs from embryonic blood progenitors.

Trophic niches of native and nonnative fishes along a river-reservoir continuum.

Instream barriers can constrain dispersal of nonnative fishes, creating opportunities to test their impact on native communities above and below these barriers. Deposition of sediments in a river inflow to Lake Powell, USA resulted in creation of a large waterfall prohibiting upstream movement of fishes from the reservoir allowing us to evaluate the trophic niche of fishes above and below this barrier. We expected niche overlap among native and nonnative species would increase in local assemblages downstream of the barrier where nonnative fish diversity and abundance were higher.

Robust Transcriptional Response to Heat Shock Impacting Diverse Cellular Processes despite Lack of Heat Shock Factor in Microsporidia.

The majority of fungal species prefer the 12° to 30°C range, and relatively few species tolerate temperatures higher than 35°C. Our understanding of the mechanisms underpinning the ability of some species to grow at higher temperatures is incomplete. is an obligate intracellular fungal parasite that infects honey bees and can cause individual mortality and contribute to colony collapse.

The heat shock response and humoral immune response are mutually antagonistic in honey bees.

The honey bee is of paramount importance to humans in both agricultural and ecological settings. Honey bee colonies have suffered from increased attrition in recent years, stemming from complex interacting stresses. Defining common cellular stress responses elicited by these stressors represents a key step in understanding potential synergies.

Divergent forms of endoplasmic reticulum stress trigger a robust unfolded protein response in honey bees.

Honey bee colonies in the United States have suffered from an increased rate of die-off in recent years, stemming from a complex set of interacting stresses that remain poorly described. While we have some understanding of the physiological stress responses in the honey bee, our molecular understanding of honey bee cellular stress responses is incomplete. Thus, we sought to identify and began functional characterization of the components of the UPR in honey bees.

Quantitative characterization of quantum dot-labeled lambda phage for Escherichia coli detection.

We characterize CdSe/ZnS quantum dot (QD) binding to genetically modified bacteriophage as a model for bacterial detection. Interactions among QDs, lambda (lambda) phage, and Escherichia coli are examined by several cross-validated methods. Flow and image-based cytometry clarify fluorescent labeling of bacteria, with image-based cytometry additionally reporting the number of decorated phage bound to cells.

Molecular characterization of a variant of Bacillus anthracis-specific phage AP50 with improved bacteriolytic activity.

The genome sequence of a Bacillus anthracis-specific clear plaque mutant phage, AP50c, contains 31 open reading frames spanning 14,398 bp, has two mutations compared to wild-type AP50t, and has a colinear genome architecture highly similar to that of gram-positive Tectiviridae phages. Spontaneous AP50c-resistant B. anthracis mutants exhibit a mucoid colony phenotype.

High-sensitivity bacterial detection using biotin-tagged phage and quantum-dot nanocomplexes.

With current concerns of antibiotic-resistant bacteria and biodefense, it has become important to rapidly identify infectious bacteria. Traditional technologies involving isolation and amplification of the pathogenic bacteria are time-consuming. We report a rapid and simple method that combines in vivo biotinylation of engineered host-specific bacteriophage and conjugation of the phage to streptavidin-coated quantum dots.

Inflammatory mediators and skeletal muscle injury: a DNA microarray analysis.

Traumatic skeletal muscle injury causes a specific sequence of cellular events consisting of degeneration, inflammation, regeneration, and fibrosis. The role of early posttraumatic mechanisms, including acute inflammatory response, in muscle repair is not well understood. In the present study, oligonucleotide microarray analyses were used to examine the candidate genes that are involved in these early events of the muscle injury/repair process.

Physiological role of tumor necrosis factor alpha in traumatic muscle injury.

degenerative and regenerative roles of tumor necrosis factor alpha (TNF-alpha), a pro-inflammatory cytokine with pleiotropic functions, were investigated by using TNF receptor 1 and 2 double knockout (TNFR-DKO) and TNF-alpha antibody neutralized mice following traumatic freeze injury to the tibialis anterior muscle. In wild-type control mice, TNF-alpha mRNA transcripts and protein increased following injury and gradually returned to control (uninjured) levels by 13 days. A reduction in MyoD mRNA expression occurred in TNF-alpha-deficient mice, although there were no visible differences in MyoD immunostaining or histological characteristics in regenerating muscles.

Bone-directed expression of Col1a1 promoter-driven self-inactivating retroviral vector in bone marrow cells and transgenic mice.

Gene therapy of bone would benefit from the availability of vectors that provide stable, osteoblast-specific expression. This would allow bone-specific expression of Col1a1 cDNAs for treatment of osteogenesis imperfecta. In addition, such a vector would restrict expression of secreted therapeutic proteins to the bone-synthesizing regions of the bone marrow after ex vivo transduction of marrow stromal cells and reintroduction of the cells into patients.

Association of tumor necrosis factor-alpha and interleukin-1 gene polymorphisms with silicosis.

Silicosis, an interstitial lung disease prevalent among miners, sand blasters, and quarry workers, is manifested as a chronic inflammatory response leading to severe pulmonary fibrotic changes. Proinflammatory cytokines, such as TNFalpha and IL-1, produced in the lung by type II epithelial cells and alveolar macrophages, have been strongly implicated in the formation of these lesions. Recently, a number of single nucleotide polymorphisms (SNPs), which quantitatively affect mRNA synthesis, have been identified in the TNFalpha promoter and IL-1 gene cluster and their frequency is associated with certain chronic inflammatory diseases.

Tracking COL1A1 RNA in osteogenesis imperfecta. splice-defective transcripts initiate transport from the gene but are retained within the SC35 domain.

This study illuminates the intra-nuclear fate of COL1A1 RNA in osteogenesis imperfecta (OI) Type I. Patient fibroblasts were shown to carry a heterozygous defect in splicing of intron 26, blocking mRNA export. Both the normal and mutant allele associated with a nuclear RNA track, a localized accumulation of posttranscriptional RNA emanating to one side of the gene.

Premature termination codon in the aggrecan gene of nanomelia and its influence on mRNA transport and stability.

Aim: To analyze the influence of the premature termination codon on mRNA transport and stability

Methods: Chondrocyte mRNA was isolated from homozygous and heterozygous nanomelic 17-days old embryos and examined by RT-PCR analysis. To analyze aggrecan mRNA stability, mRNA synthesis was inhibited with DRB [5,6 dichloro-1-(-D-ribofuranosyl benzimidazole)], a specific inhibitor of RNA polymerase II. Visualization of the aggrecan alleles was performed by in situ hybridization.

The signal transduction pathway of CD23 (Fc epsilon RIIb) targets I kappa B kinase.

Alveolar macrophages play a crucial role in initiating the inflammatory response in allergic asthma through the cross-linking of the low affinity IgE receptors (Fc epsilon RIIb or CD23) by IgE-allergen immunocomplexes. We have previously shown that CD23 cross-linking in monocytes and U937 cells targets I kappa B alpha, leading to the activation of the transcription factor NF-kappa B. We demonstrate in this paper that CD23-initiated signaling in U937 cells leads to hyperphosphorylation of I kappa B alpha at Ser32/Ser36 residues.

Signal transduction pathways triggered by the FcepsilonRIIb receptor (CD23) in human monocytes lead to nuclear factor-kappaB activation.

Background: Alveolar macrophages play a key role in the initiation of the inflammatory reaction of allergic asthma. Alveolar macrophages and peripheral blood monocytes are activated when IgE/allergen immune complexes bind to the CD23 receptor, which leads to the production of inflammatory cytokines.

Objective: We sought to investigate the molecular mechanisms regulating this early inflammatory response.

RESEARCH: Attitudes of Private- and Public-Land Managers in Wyoming, USA, Toward Beaver.

/ A mail survey concerning beaver (Castor canadensis) management in Wyoming, USA, was sent to 5265 private-land managers and 124 public-land managers during 1993. The survey was developed in response to increasing interest in beaver management and beaver reintroduction possibilities. Private-land managers responding to the survey supplied information on 62,859 km2 of land area and 20,037 km of streams.

Nuclear retention of COL1A1 messenger RNA identifies null alleles causing mild osteogenesis imperfecta.

Osteogenesis imperfecta (OI) is a heritable connective tissue disorder characterized by bone fragility. Most cases of severe OI result from mutations in the coding region of the COL1A1 or COL1A2 genes yielding an abnormal collagen alpha chain. In contrast, many patients with mild OI show evidence of a null allele due to a premature stop mutation in the mutant RNA transcript.

Defective splicing of mRNA from one COL1A1 allele of type I collagen in nondeforming (type I) osteogenesis imperfecta.

Osteogenesis imperfecta (OI) type I is the mildest form of heritable bone fragility resulting from mutations within the COL1A1 gene. We studied fibroblasts established from a child with OI type I and demonstrated underproduction of alpha 1 (I) collagen chains and alpha 1 (I) mRNA. Indirect RNase protection suggested two species of alpha 1 (I) mRNA, one of which was not collinear with fully spliced alpha 1 (I) mRNA.