Post-fire vegetation response at the woodland-shrubland interface is mediated by the pre-fire community

Understanding the drivers of ecosystem responses to disturbance is essential for management aimed at maintaining or restoring ecosystem processes and services, especially where invasive species respond strongly to disturbance. In this study, we used repeat vegetation surveys from a network of prescribed fire treatments at the woodland-shrubland interface in the Shoshone Mountains, Nevada, USA, to investigate post-fire responses of the understory plant community. First, we characterized post-fire community trajectories for sites located along an elevational gradient, hypothesizing a positive relationship between elevation and resistance to invasion. Unburned understory communities and their responses to disturbance differed along the gradient. As hypothesized, lower elevations experienced greater species turnover and higher invasive annual grass (Bromus tectorum) cover after fire. Second, we characterized post-fire plant community trajectories for sites with varying levels of pre-fire pinyon and juniper cover, hypothesizing that pre-fire tree dominance and associated reductions in perennial understory species lead to less predictable post-fire trajectories. Among sites with low-to-moderate tree cover, burning largely eliminated differences in understory composition, suggesting that biotic legacies were sufficient to result in predictable trajectories. In contrast, sites with high pre-fire tree cover transitioned into an annual forb-dominated community with sparse vegetation cover, suggesting that the loss of the understory community initiated unpredictable and divergent post-fire trajectories. Because plant communities were still changing four years after fire, it is unclear whether the alternate trajectories in sites with high tree cover will result in the formation of alternate states, or whether community composition will eventually converge with other sites at the same elevation. Results indicate that careful evaluation of site characteristics can be used to predict treatment outcomes at the woodland-shrubland interface, and to guide the appropriate use of prescribed fire or other management practices

Three unidentified men in a gallery

three young men in a galler

Painting 1960's

Students in painting class 1960

Graduate Division students

Image of Graduate Divsion students in class from CCAC Bulletin, 196

Students on benches in front of the dorms

Image of students on benches in front of the dorms from CCAC Bulletin, 196

Genomic Loss and Epigenetic Silencing of the FOSL1 Tumor Suppressor Gene in Radiation-induced Neoplastic Transformation of Human CGL1 Cells Alters the Tumorigenic Phenotype In Vitro and In Vivo

The CGL1 human hybrid cell system has been utilized for many decades as an excellent cellular tool for investigating neoplastic transformation. Substantial work has been done previously implicating genetic factors related to chromosome 11 to the alteration of tumorigenic phenotype in CGL1 cells. This includes candidate tumor suppressor gene FOSL1, a member of the AP-1 transcription factor complex which encodes for protein FRA1. Here we present novel evidence supporting the role of FOSL1 in the suppression of tumorigenicity in segregants of the CGL1 system. Gamma-induced mutant (GIM) and control (CON) cells were isolated from 7 Gy gamma-irradiated CGL1s. Western, Southern and Northern blot analysis were utilized to assess FOSL1/FRA1 expression as well as methylation studies. GIMs were transfected to re-express FRA1 and in vivo tumorigenicity studies were conducted. Global transcriptomic microarray and RT-qPCR analysis were used to further characterize these unique cell segregants. GIMs were found to be tumorigenic in vivo when injected into nude mice whereas CON cells were not. GIMs show loss of Fosl/FRA1 expression as confirmed by Western blot. Southern and Northern blot analysis further reveals that FRA1 reduction in tumorigenic CGL1 segregants is likely due to transcriptional suppression. Results suggest that radiation-induced neoplastic transformation of CGL1 is in part due to silencing of the FOSL1 tumor suppressor gene promoter by methylation. The radiation-induced tumorigenic GIMs transfected to re-express FRA1 resulted in suppression of subcutaneous tumor growth in nude mice in vivo. Global microarray analysis and RT-qPCR validation elucidated several hundred differentially expressed genes. Downstream analysis reveals a significant number of altered pathways and enriched Gene Ontology terms genes related to cellular adhesion, proliferation, and migration. Together these findings provide strong evidence that FRA1 is a tumor suppressor gene deleted and epigenetically silenced after ionizing radiation-induced neoplastic transformation in the CGL1 human hybrid cell system